Articles in 2024

Döring, van der Vorst, Yan, Neideck et al. present a non-canonical chemokine pathway involving CCL17 signaling through CCR8, which induces CCL3 expression independent of CCR4 and suppresses the functions of atheroprotective T_reg cells.

Carramolino et al. show that fibromyocytes and chondromyocytes are selectively depleted, while cap cells are maintained, in regressing mouse plaques.

Goerlich et al. review the current knowledge of the cardiovascular complications of the post-COVID condition, including postural orthostatic tachycardia syndrome, myocardial injury, heart failure, myocarditis and arrhythmias, highlighting currently available and potential treatments.

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.

In the USA, scientific merit is the main criterion determining funding for biomedical research, but not for the institutional space or support needed to perform it. Realigning the incentives of academic institutions with those of funding sources could produce better science.

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 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.

In acute myocardial infarction treated with reperfusion, functional preservation of myocardium requires an angiogenic response. A new study shows that CRELD2, an endoplasmic reticulum (ER)-resident protein induced in response to ER stress, acts as an angiocrine factor to limit cardiac dysfunction after ischemia/reperfusion injury in mice.

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.

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.

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.

Wu et al. profile the secretome of cardiac endothelial cells exposed to endoplasmic reticulum (ER) stress during acute myocardial infarction and identify CRELD2 as an angiogenic growth factor supporting infarct repair.

Shetty et al. report that individuals of African ancestry harboring a high-proportion spliced-in titin truncating variant have a similar increase in the risk of atrial fibrillation, dilated cardiomyopathy and heart failure as individuals of European ancestry.

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.

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.

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.