Haykin et al. show that activation of the brain’s reward system modulates adrenergic input to the liver and complement component 3 transcription, affecting vascularization and improving cardiac recovery after acute myocardial infarction.

Selvakumar, Clayton et al. use a porcine model of myocardial infarction and PSC-CM transplantation and identify atrial and pacemaker-like cardiomyocytes as the cause of engraftment arrhythmias and surface marker signatures to distinguish between arrhythmogenic and non-arrhythmogenic cardiomyocytes.

Fleetwood et al. review the role of immune cell dysfunction and inflammation in cardiovascular diseases. Their Review explores immune cell metabolic reprogramming in response to environmental cues, offering insights into potential therapeutic strategies for cardiovascular diseases.

Hartman et al. use mouse models of cardiac function to show that aficamten decreases the availability of myosin heads for contraction during systole, attenuating a primary driver of hypertrophic cardiomyopathy pathophysiology.

Doan et al. show that loss of cardiac NAD⁺ is sufficient to drive metabolic derangements, hypertrophic remodeling and lethal arrhythmias in adult mouse hearts, despite maintenance of ejection fraction and bioenergetics.

By integrating DNA genotype and RNA sequencing data from human samples, d’Escamard et al. identify a gene regulatory co-expression supernetwork that plays an important role in fibromuscular dysplasia, a poorly understood disease affecting 3–5% of adult females.

Goumenaki et al. uncover that during zebrafish cardiac regeneration, MyD88 signaling promotes the inflammatory response to injury and attenuates the endocardial-mediated fibrotic response.

Joshi et al. show that γ-protocadherins suppress the anti-inflammatory KLF2 and KLF4 pathway and that targeting them is a viable therapeutic strategy to protect against atherosclerosis.

Yu Shi et al. show that the citric acid cycle metabolite α-ketoglutarate promotes cardiomyocyte proliferation during heart development and promotes heart regeneration after myocardial infarction.

Boulgakoff et al. show that during cardiac regeneration, ventricular trabeculae participate in the repair of the contractile myocardium resulting in an excessive production of immature Purkinje fibers forming a hyperplastic PF network and altered ventricular conduction.

This summer, we have witnessed several high-level sports events, the UEFA European Football Championship, the Tour de France/Tour de France Femmes and the Olympic Games. As we admired these impressive athletic performances, the issue of performance-enhancing drugs (PEDs) inevitably resurfaced. Although PEDs are sometimes used to treat cardiovascular diseases, they can also cause severe side effects such as atherosclerosis, thrombosis, arrhythmias and sudden cardiac death. Here we discuss the use of PEDs, their direct effects and side effects on the cardiovascular system with Aaron Baggish, a professor of medicine at the University of Lausanne’s Institut des Sciences du Sport (ISSUL), chief of sports cardiology at the Centre Hospitalier Universitaire Vaudois (CHUV), and founder and emeritus director of the Massachusetts General Hospital Cardiovascular Performance Program (CPP) affiliated with Harvard Medical School. Baggish has been working with athletes for over 10 years and is a consultant for numerous sports and sports-related organizations including the World Anti-Doping Agency (WADA).