Cardiac hypertrophy articles from across Nature Portfolio

Glycoprotein non-metastatic melanoma protein B (GPNMB) is produced by macrophages and mediates cardiac repair through direct interaction with an orphan G-protein-coupled receptor, GPR39.

L. Zhang, M. Zhang, Huang et al. show that Klf9 regulated PGC-1α and Mfn2 expression, contributing to mitochondrial energy metabolism and dynamic regulation, promoting mitophagy, improving cardiac function and revealing a potential therapeutic target.

Ramadoss et al. show that bone-marrow-derived macrophages contribute to heart repair following myocardial infarction by secreting GPNMB, which binds to the orphan receptor GPR39 to improve myocyte contractility and reduce fibroblast activation.

The cardiac conduction system dictates the pacing of the heartbeat, but despite its importance relatively little is known about the mechanisms underlying its development. Here they show that the G4 resolvase Dhx36 is important for regulating cardiac conduction system morphogenesis and function.

Glycoprotein non-metastatic melanoma protein B (GPNMB) is produced by macrophages and mediates cardiac repair through direct interaction with an orphan G-protein-coupled receptor, GPR39.

Aficamten, a small-molecule myosin inhibitor, binds to the catalytic domain of cardiac myosin and reduces contraction by stabilizing the initial weak interaction between myosin and actin.

Diabetes can cause heart failure by a toxic accumulation of lipids in cardiac myocytes, which impairs their function. This work shows that stimulation of the bile acid receptor TGR5 limits fatty acid uptake into cardiac myocytes and prevents the development of diabetic cardiomyopathy.

According to data from the IMPROVE-HCM trial, ninerafaxstat is well tolerated by patients with symptomatic non-obstructive hypertrophic cardiomyopathy and improves exercise performance among those who are most symptomatically limited.

Myocarditis, an inflammatory heart disease, causes cardiomyocyte loss leading to heart failure. Research now shows that BMP4 is crucial for cardiac tissue homeostasis, and targeted neutralization of BMP inhibitors GREM1 and GREM2 mitigates T cell-induced myocardial inflammation and maintains cardiomyocyte integrity.