Volume 3 Issue 1, January 2024

The European Research Council (ERC) provides opportunities each year for researchers to apply for various grant programs to fund their research. One of these grant categories is the ERC Starting Grant, which is specifically designed for early-career scientists who are prepared to work independently. This grant is open to researchers from any field and any nationality provided that they have 2–7 years of experience since completing their PhD and are conducting their research at public or private research organizations in EU member states or associated countries. The competition for this prestigious funding opportunity is fierce, but successful projects can receive up to €1.5 million for a period of 5 years.

The Leducq Foundation is a not-for-profit grant-making organization that has been fostering transatlantic collaboration in the cardiovascular field for two decades. Here we learn more about the history of the foundation, its ongoing projects, and its impacts on the cardiovascular field in conversation with David Tancredi, who has had an executive role with the Leducq organization for over 20 years, and with Connie R. Bezzina and Mete Civelek, who are coordinators of two financed networks of excellence.

The European Research Council (ERC) provides opportunities each year for researchers to apply for various grant programs to fund their research. One of these grant categories is the ERC Starting Grant, which is specifically designed for early-career scientists who are prepared to work independently. This grant is open to researchers from any field and any nationality provided that they have 2–7 years of experience since completing their PhD and are conducting their research at public or private research organizations in EU member states or associated countries. The competition for this prestigious funding opportunity is fierce, but successful projects can receive up to €1.5 million for a period of 5 years.

The European Research Council (ERC) provides opportunities each year for researchers to apply for various grant programs to fund their research. One of these grant categories is the ERC Starting Grant, which is specifically designed for early-career scientists who are prepared to work independently. This grant is open to researchers from any field and any nationality provided that they have 2–7 years of experience since completing their PhD and are conducting their research in public or private research organizations in EU member states or associated countries. The competition for this prestigious funding opportunity is fierce, but successful projects can receive up to €1.5 million for a period of 5 years.

The European Research Council (ERC) provides opportunities each year for researchers to apply for various grant program to fund their research. One of these grant categories is the ERC Starting Grant, which is specifically designed for early-career scientists who are prepared to work independently. This grant is open to researchers from any field and any nationality provided that they have 2–7 years of experience since completing their PhD and are conducting their research in public or private research organizations in EU member states or associated countries. The competition for this prestigious funding opportunity is fierce, but successful projects can receive up to €1.5 million for a period of 5 years.

Pro-reparative cardiac-resident macrophages have emerged as major players in salvaging the ischemic myocardium of a diseased heart. New research now highlights ATF3 as a key transcription factor that governs macrophage survival and proliferation and myocardial repair.

Timothy syndrome is a severe variant of long QT syndrome, but an accurate in vivo model to study the disease and identify treatments has been lacking. A knock-in swine model of Timothy syndrome now shows that CaMKII-mediated reduction in peak I_Na slows the cardiac impulse propagation and contributes to the severe arrhythmia in the disorder.

Physical simulators of organs can have great impact on diagnostic and surgical training. A novel biohybrid platform to simulate the right ventricle of the heart with high fidelity has been developed and tested, demonstrating that this is a valid alternative to in vivo experimentation.

Clonal hematopoiesis of indeterminate potential (CHIP) is a risk factor for cardiovascular disease. Neutralization of the cytokine IL-1β (as in the CANTOS clinical trial) resulted in a greater reduction in adverse cardiovascular events in patients with CHIP than the reduction in molecularly unstratified patients. New research reveals that some of the cardiovascular benefits of anti-IL-1β therapy in patients with CHIP might be delivered by an improvement in plaque stability via increased fibroblast-like cells.

GPR15 is a chemoattractant-G protein-coupled receptor that mediates homing of T cells. Stoffers et al. present insights into how GPR15 mediates the recruitment of cytotoxic T cells to contain and clear coxsackievirus B3 from the heart and regulatory T cells to limit immune pathology.

Shao, Li, Liu et al. identify the GAS6–ATF3 axis as a central regulator of survival and proliferation of protective resident MerTK⁺ cardiac macrophages and show that GAS6 administration improves cardiac repair after ischemic–reperfusion injury in mice in an ATF3-dependent manner.

Lhoste et al. show that cardiometabolic and renal traits of the US population have shifted from phenotypes with high blood pressure and high cholesterol toward poor kidney function, hyperglycemia and severe obesity.

Fidler et al. show that anti-IL-1β treatment of atherosclerotic Ldlr-null mice with clonal expansion of Tet2-null or Jak2^VF hematopoietic stem cells promotes the recruitment of fibroblast-like cells to the plaque fibrous cap, leading to cap thickening and increased plaque stability. Conversely, the removal of fibroblast-like cells during atherosclerosis progression results in reduced fibrous cap formation in mice receiving anti-IL-1β antibody treatment.

Stoffers, Wolf et al. report that, in virus-mediated myocarditis, GPR15 deficiency delays the recruitment of T cells into cardiac tissue, which impairs viral elimination and leads to delayed but also prolonged inflammation and, thus, adverse cardiac outcomes.