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PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

Research group: The candidate will join a multidisciplinary research group including clinical and basic scientists. The group has an extensive trajectory of more than 20 years in heart failure, focused on myocardial remodeling and the validation of blood biomarkers. The supervisor, Dr. González, has participated in 130 scientific publications and the group has been involved in over 50 research projects, including National and collaborative European Commission-funded projects (FP7, H2020, ERA-NET) and contracts with pharmaceutical companies. 

Research project: Heart failure (HF) is one of the leading causes of death and hospitalization. HF with preserved ejection fraction (HFpEF), with increasing prevalence given its association with risks factors such as hypertension, diabetes and aging, remains poorly understood and lacks specific diagnostic and therapeutic strategies. Microvascular dysfunction and the associated cardiac inflammation have been proposed as key players leading to myocardial remodeling and cardiac dysfunction in HFpEF. Of note, one of the hallmarks of myocardial remodeling in HFpEF is the development of diffuse interstitial fibrosis, which increases the stiffness of the cardiac tissue. However the pathophysiological mechanisms mediated by microvascular dysfunction, and in particular its association with fibrosis, need to be further studied. On the other hand, there is an unmet need to develop sensitive tools for the non-invasive assessment of myocardial microvascular dysfunction (by either cardiac imaging techniques or blood biomarkers). 

This translational project is focused on: 1) Understanding the contribution of microvascular dysfunction to cardiac inflammation, myocardial fibrosis and cardiac dysfunction in patients at different stages of evolution of HFpEF and in experimental models; 2) Validating novel imaging biomarkers of myocardial microvascular dysfunction by cardiac magnetic resonance; 3) Identifying novel blood biomarkers derived from endothelial cells microvesicles by next generation sequencing (mRNA-Seq).

Candidate description: The fellow is expected to enroll in a PhD programme at the Universidad de Navarra.

He/She will become a member of a leading research group, which follows a translational approach to understand the mechanisms involved in HF development, aiming at identifying new diagnostic tools and therapeutic strategies. Moreover, the project will involve interaction with international collaborators of ongoing related projects and a short term stay in a European-based research lab within the group network.

A bachelor and a master in Biomedical Sciences (e.g. biology, biochemistry, pharmacy, medicine, biomedicine…) is required. 
The fellow must be fluent in English (both oral and written). Previous experience in histology, cell biology, RNA analysis and biostatistics is recommended but not essential. 

The candidate will benefit from a multidisciplinary training to understand the pathophysiology of HFpEF and the current clinical gaps in diagnosis and management, as well as from obtaining the technical skills required. 

Interested applicants should send a cover letter describing past experience and interests as well as their CV to:
Arantxa González Miqueoamiqueo@unav.es

PI: Susana Ravassa

Chronic heart failure is a heterogeneous syndrome, the end result of diverse pathophysiological mechanisms and different histocellular alterations.

In order to design personalized therapeutic strategies aimed at correcting the predominant alterations in each patient, it is necessary to have precise biomarkers that allow early diagnosis, better risk stratification in patients and monitoring of the effects of therapy. 

Since obtaining endomyocardial biopsies is not feasible on a large scale, circulating and imaging biomarkers are a useful tool for the analysis of large patient populations. In recent years we have defined a panel of biomarkers of myocardial remodeling that includes markers of fibrosis (PICP and CITP:MMP-1), cardiomyocyte damage and stress (NT-proBNP and hs-TnT) and inflammation (IL-18, sST-2, galectin-3).

Similarly, advances in cardiac magnetic resonance have allowed the development of new parameters to assess microvascular alterations and diffuse myocardial fibrosis.

This project focuses on analyzing the diagnostic and therapeutic usefulness of the panel of biomarkers of myocardial remodeling and identifying new molecular biomarkers to define molecular profiles corresponding to the different phenotypes of patients with chronic heart failure.

Objectives

  1. To establish a profile of circulating and cardiac imaging biomarkers that reflect the different aspects of myocardial remodeling. Biomarkers already identified will be combined with new biomarkers under development, derived from proteomic studies and characterization of non-coding RNAs.
  2. To assess the diagnostic and prognostic utility of the panel of biomarkers of myocardial remodeling in patients with chronic heart failure of different etiologies and different associated pathologies (atrial fibrillation, chronic kidney disease...).
  3. To analyze the usefulness of the myocardial remodeling biomarker panel for monitoring the effects of therapy in patients with chronic heart failure and associated pathologies.
  4. To use the myocardial remodeling biomarker panel to detect cardiovascular sequelae in patients with cardiotoxicity induced by chemotherapeutic agents or in patients infected with Sars-CoV-2.

PI: Mª Ujué Moreno Zulategui

In recent years it has been demonstrated that extracellular vesicles (EVs) are actively released in response to tissue damage, so that the analysis of both their number and content can provide valuable information both in terms of the identification of new biomarkers and new pathophysiological mechanisms. In fact, it has been proposed that EVs may act as mediators by transferring their content (proteins, non-coding RNAs or mRNAs) to target cells in a paracrine or endocrine manner.

The optimization of massive sequencing technologies (NGS) for serum and plasma studies has allowed the characterization of the transcriptome of EVs present in plasma, as well as the analysis of circulating non-coding RNAs.

This approach will make it possible to establish molecular profiles associated with the different phenotypes of chronic heart failure, which may also be pathophysiological mediators, and to lay the foundations for the identification of new therapeutic targets.

Objectives

  1. To characterize the cellular origin (endothelial, platelet, cardiomyocyte, leukocyte) of plasma EVs in patients with chronic heart failure of different etiologies and at different stages of evolution.
  2. To identify new biomarkers by analyzing the transcriptome (mRNA-Seq) of plasma EVs in patients with chronic heart failure and their associated co-morbidities (chronic kidney disease, atrial fibrillation).
  3. To validate the pathophysiological relevance of targets identified in the analysis of the transcriptome of EVs in cellular and animal models.
  4. To evaluate the transcriptome of endothelial-derived EVs to assess the implication of microvascular alterations as a common causal mechanism in chronic heart failure with preserved ejection fraction and cognitive impairment.
  5. To establish new biomarkers based on the analysis of the serum microRNA-ome in patients with chronic heart failure of different etiologies and at different stages of evolution.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

We are seeking for a creative, ambitious and highly motivated Postdoc candidate to join a fully funded project within the Hematology-Oncology Program at CIMA Universidad de Navarra.

The candidate will join a highly collaborative environment with the opportunity to apply cutting-edge genomic technologies on the field of Hematology Oncology. The work will be in permanent collaboration with an interactive international team of basic and translational researchers.

The successful candidate will:

  • Work in a unique team of experts in Multiple Myeloma

  • Participate in high impact projects involving next generation sequencing experiments for the study of gene regulation and epigenetics (RNA-seq, ChIP-seq, ATAC-seq, HI-C, single cell RNA-seq, etc.), flow cytometry and cellular and molecular studies.

  • Analyze and integrate cancer genomic data.

  • Participate in the development of data analysis workflows and pipelines for high throughput “omics” data.

  • Collaborate in multiple projects, having the possibility to carry on a personal research project.

  • Collaborate with the development of any bioinformatic necessary tools to accomplish goals.

  • Be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules

  • Co-supervise PhD and Master students

  • Participate in the oral presentation of all project findings and abstracts including participation in periodic project status meetings and presentation of final project deliverables

Required qualifications:

  • PhD training in molecular and cellular biology with skills in NGS and flow cytometry techniques and/or Multiple Myeloma.

  • Experience in sample processing, cellular and molecular biology.

  • Animal handling experience.

  • Excellent interpersonal skills (project management, English and communication –oral and written-, motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…).

  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Applicants are encouraged to apply for competitive fellowship awards. Salary will be commensurate with qualifications and experience.

Interested applicants should send a cover letter describing past experience and interests as well as their CV including references to:

Oscar González
ogonmor@unav.es
T + 34 948 194 700 ext 811047

Location: Regenerative Medicine Program. CIMA, Navarra (Spain)

Contract: Technician position, full time, for 1 year and 3 months. The position is available from 11th of January 2021

Application process: applicants must send to Xabier Aranguren (xlaranguren@unav.es) a cover letter describing experience and research interests, and an up-to-date CV. 

Project scope: 

Inter-species chimera generation and transgenesis in a pig model

Candidates with the following expertises will be preferred:

  • Training in molecular and cellular biology: CRISPR/Cas9 technology, stem cell cultures
  • Animal handling experienc

Location: Gene Therapy and Regulation of Gene Expression Program. CIMA, research Center of the University of Navarra and Clínica Universidad de Navarra (CUN).

Contract: Postdoctoral position, full time, for 8 months with possibility of renewal

Application process: applicants must send to Puri Fortes (pfortes@unav.es) a cover letter describing experience and research interests, and an up-to-date CV including the name and addresses of three former mentors for reference letters.

Project scope: The position is available from November 1st, 2020 for the development of novel therapies for hepatocellular carcinoma (HCC) targeting long non-coding RNAs

The successful candidate will:

  • work in an unique team of experts in functional RNAs
  • use up-to-date models for nucleic acid delivery in vitro and in vivo
  • develop preclinical models for HCC
  • co-supervise PhD and Master students
  • be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules
  • collaborate with basic researchers in biotechnology and functional RNAs and bioinformaticians at CIMA and with clinical researchers at CUN

Qualifications to be considered

  • PhD training in molecular and cellular biology with skills in RNA techniques and/or HCC
  • Animal handling experience
  • Excellent interpersonal skills (project management, English and communication –oral and written-, motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…)
  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Applicants are encouraged to apply for competitive fellowship awards.
  • Salary will be commensurate with qualifications and experience.

Location: Gene Therapy and Regulation of Gene Expression Program. CIMA, research Center of the University of Navarra.

Contract: Technician position, full time, for 6 months
Application process: applicants must send to Puri Fortes (pfortes@unav.es) a cover letter describing experience and research interests, and an up-to-date CV including the name and addresses of three former mentors for reference letters. 

Project scope: The position is available from November 1st, 2020 for the evaluation of gene expression in mouse models using up-to-date technology

The successful candidate will

  • Work in an unique team of experts liver cancer and functional RNAs
  • Use up-to-date models for nucleic acid delivery in vitro and in vivo
  • Be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules
  • Collaborate with basic researchers in biotechnology and functional RNAs and bioinformaticians at CIMA and with clinical researchers at CUN

Qualifications to be considered

  • Training in molecular and cellular biology
  • Animal handling experience
  • Excellent interpersonal skills (motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…)
  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Salary will be commensurate with qualifications and experience.

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