Inhibition of mitochondrial sodium/calcium exchanger, NCLX, as a therapeutic strategy to reduce myocardial ischemia-reperfusion injury during myocardial infarction VHIR is seeking an outstanding and highly motivated postdoctoral researcher to apply for a Marie Sklodowska-Curie Postdoctoral Fellowship in the field of mitochondrial biology, cardiovascular pathophysiology and translational cardio protection.

Marie Skłodowska-Curie Actions – Postdoctoral Fellowships (MSCA-PF) 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 .

Full eligibility details: MSCA Postdoctoral Fellowships 2026 Background Myocardial ischemia-reperfusion (IR) injury remains a major challenge in cardiovascular medicine. While rapid reperfusion improves survival after myocardial infarction, it paradoxically triggers additional myocardial damage, promoting infarct expansion and heart failure. Mitochondria play a central role via disruptions in energetics, calcium handling, and excessive reactive oxygen species (ROS) production.

Recent studies identify the mitochondrial sodium/calcium exchanger NCLX (SLC8B1) as a key regulator of mitochondrial ROS signalling, linking sodium influx to electron transport chain dysfunction during hypoxia/reoxygenation. Notably, NCLX inhibition reduces ROS and tissue damage in cerebral ischemia models, suggesting a novel role for mitochondrial sodium in ischemic injury, still unexplored in the heart. Our preliminary data show that NCLX inhibition significantly reduces infarct size in cardiac IR models.

This project combines cutting-edge mitochondrial biology with translational cardiovascular research to uncover how NCLX controls ROS production, mitochondrial function, and cardiomyocyte survival using advanced in vitro, ex vivo, in vivo, and human models. These findings may redefine reperfusion injury mechanisms and open new therapeutic strategies for ischemic heart disease.

Objective The goal of this project is to determine whether the mitochondrial sodium/calcium exchanger NCLX is a key regulator of reactive oxygen species (ROS) production and myocardial injury during ischemia-reperfusion (IR), and to assess the therapeutic potential of its inhibition in acute myocardial infarction.

The project will examine how NCLX controls mitochondrial sodium and calcium balance, respiratory chain function, and ROS generation during ischemia and reperfusion, as well as the molecular mechanisms linking NCLX activity to mitochondrial dysfunction and cardiomyocyte death. In parallel, the cardioprotective efficacy of novel NCLX inhibitors will be tested in isolated hearts, and in vivo rodent and pig models.

By integrating mechanistic and translational approaches, this work aims to establish mitochondrial Na+/Ca2+ exchange as a novel therapeutic target in ischemic heart disease. Our Group The research group focuses on the molecular and translational mechanisms underlying cardiovascular disease, with particular expertise in myocardial ischemia-reperfusion injury, heart failure, adverse ventricular remodelling and cardiac arrhythmias.

Its main research lines include the study of mitochondrial and cellular mechanisms of ischemia-reperfusion injury, heart failure progression, inflammatory signalling, cardiovascular aging and metabolic stress, as well as the impact of environmental factors such as air pollution on cardiac function. The group integrates mechanistic research in mitochondrial biology, redox signalling, calcium handling and inflammation with translational approaches using cellular systems, isolated organs, rodent and porcine models, and human cardiac samples.

Main responsibilities and duties: Conduct high‑quality research aligned with project and lab objectives, including rigorous data collection, analysis, and literature review. Collaborate with senior researchers in designing experiments, developing research protocols, and contributing to publications, reports, and grant proposals. Present research findings within the team and at scientific conferences or seminars. Provide guidance to junior researchers or graduate students and supervise Bachelor’s and Master’s students when applicable.

Engage in continuous professional development and work with the technology transfer office to identify potential inventions and understand IP processes.