Sayers et al. reveal that heart regeneration during the neonatal period in mice extends to conduction system restoration after insult, highlighting the difference between this process and pathological remodeling in the adult heart.

Maatz, Lindberg et al. identify molecular alterations and immune response changes in endomyocardial biopsies from patients with myocarditis after COVID-19 infection, after anti-COVID-19 vaccination or from non-COVID-related causes.

Using single-cell and spatial molecular profiling of infarcted mouse and human hearts, Li, Ni, Wang and colleagues identify a subset of cardiac fibroblasts expressing CD248 that plays a critical role in fibroblast–T cell interaction, and show that disrupting this interaction with monoclonal antibodies or anti-CD248 chimeric antigen receptor T cells results in reduced cardiac fibrosis and improved function.

Lai et al. present a spatially resolved atlas of human atherosclerotic plaques, revealing cellular heterogeneity and identifying lymphoid structures and their potential functions and implications.

Freundt, Hartmann and colleagues use a multimodal approach to show that titin cleavage impairs ventricular filling and reduces chamber size by disrupting elastic recoil, promotes fibroblast activation and ultimately drives decompensated heart failure, supporting a function of titin as a mechanical stress sensor.

Julian et al. combine machine learning and multi-omic analyses using UK Biobank data to link ophthalmic image features to cardiovascular and neurodegenerative diseases and identify relevant pathways.

Venkatesh, Cherlin et al. perform a genome-wide association study to identify variants associated with myocardial blood flow reserve as a readout of coronary microvascular function, revealing NF-kB signaling as a potential regulator.

Atallah et al. show that oxidized phospholipids and lipoprotein (a), but not systemic inflammation indicators are associated with tissue-level myocardial inflammation after infarction.

Owen et al. used single-cell RNA sequencing and spatial transcriptomics to analyze graft cells in heart transplants with cardiac allograft vasculopathy, showing that vascular smooth muscle cells and macrophages drive interferon-mediated inflammation and that JAK signaling blockade prolongs allograft survival.

Hu et al. show that the transmembrane glycoprotein CD98hc in cerebral endothelial cells regulates the integrin–FAK signaling pathway, thereby promoting angiogenesis and maintaining blood–brain barrier integrity.

Apheresis, introduced 50 years ago, remains a crucial therapy for homozygous familial hypercholesterolemia, a rare gene disorder that causes extreme LDL-cholesterol levels and early cardiovascular death. This Comment also honors the late professor Thompson, a pioneer of apheresis, whose work helped to shape the field.