VHIR-MSCA-PF-2026.001_Postdoctoral Fellowship (Cardiovascular Diseases

Puesto: VHIR-MSCA-PF-2026.001_Postdoctoral Fellowship (Cardiovascular Diseases)
Organisation/Company Fundació Hospital Universitari Vall d'Hebron
- Institut de recerca Department Research Department Research Field Biological sciences Biology Researcher Profile Recognised Researcher (R2) Positions Postdoc Positions Final date to receive applications 31 Jul 2026 - 23:59 (Europe/Andorra) Country Spain Type of Contract Temporary Job Status Full-time Is the job funded through the EU Research Framework Programme? Other EU programme Is the Job related to staff position within a Research Infrastructure?

No
Offer Description   Targeting cardiac amino acid transport and catabolic reprogramming in heart failure
VHIR is seeking an outstanding and highly motivated postdoctoral researcher to apply for a Marie Sklodowska-Curie Postdoctoral and join the Cardiovascular Research Group.
The Marie Skłodowska-Curie Postdoctoral Fellowships (MSCA-PF) are part of the Horizon Europe programme and support postdoctoral researchers in developing an original research and innovation project through international mobility.
The programme aims to strengthen researchers’ careers through excellent science, international collaboration and interdisciplinary experience, while fostering integration in both academic and non-academic environments. The MSCA-PF call is highly competitive and represents an excellent opportunity to attract international talent and support researchers in consolidating their scientific careers through an ambitious mobility-based fellowship.
The 2026 call closes on 09/09/2026 (17:00 Brussels time). For candidates applying to a European Postdoctoral Fellowship, the fellowship duration is from  12 to 24 months .
Heart failure (HF) is a leading cause of hospitalization and mortality worldwide, and current therapies only partially slow its progression. The failing heart undergoes maladaptive metabolic remodeling, with reduced substrate flexibility and a striking accumulation of branched-chain amino acids (BCAAs: leucine, isoleucine, valine) in both plasma and myocardium. Elevated BCAAs drive insulin resistance and chronic mTORC1 activation, fueling pathological hypertrophy, fibrosis and contractile dysfunction.

Recent work shows that boosting cardiac BCAA catabolism alone is insufficient to normalize myocardial BCAA content, pointing to amino acid transport, rather than intrinsic oxidation, as the key control point. Our preliminary data identify the neutral amino acid transporter Slc7a5 (LAT1) as a critical determinant of cardiac BCAA uptake: it is upregulated in failing cardiomyocytes, and cardiomyocyte-specific deletion reduces myocardial BCAA accumulation and attenuates adverse remodeling in pressure-overload models.

This opens an unexplored therapeutic axis at the intersection of cardiac metabolism, insulin signaling and HF.
Our Group
The Cardiovascular Diseases group at VHIR is a multidisciplinary team integrating basic and clinical researchers, with a long-standing track record in translational cardiovascular research, with seminal contributions to ischemia/reperfusion injury, cardioprotection and the metabolic basis of adverse cardiac remodeling and HF. The group integrates a wide range of preclinical HF models in mice, rats and pigs, cardiomyocyte and fibroblast isolation, ex vivo Langendorff perfusion, knockout mouse lines and has privileged access to ventricular biopsies and serum from cardiology patients.

A core current line is supported by several competitive grants. The team collaborates with international academic and biotech partners, providing a vibrant, multidisciplinary environment for an MSCA postdoctoral fellow.
Main responsibilities and duties:
The candidate will investigate how alterations in cardiac BCAA transport contributes to insulin resistance, adverse remodeling and HF progression,
Evaluate pharmacological and dietary strategies to correct cardiac BCAA overload.
Specific aims include:  characterise cardiac amino acid metabolic rewiring in murine HF models and in endomyocardial biopsies and serum from patients with aortic stenosis, combining UPLC-MS/MS metabolomics and RNA-seq;
dissect the role of cardiomyocyte and fibroblast Slc7a5 using inducible tissue-specific…