Prenatal inflammation exposure-programmed hypertension exhibits multi-generational inheritance via disrupting DNA methylome.

The multi-generation heredity trait of hypertension in human has been reported, but the molecular mechanisms underlying multi-generational inheritance of hypertension remain obscure. Recent evidence shows that prenatal inflammatory exposure (PIE) results in increased incidence of cardiovascular diseases, including hypertension. In this study we investigated whether and how PIE contributed to multi-generational inheritance of hypertension in rats.

α-Galactosylceramide and its analog OCH differentially affect the pathogenesis of ISO-induced cardiac injury in mice.

Immunotherapies for cancers may cause severe and life-threatening cardiotoxicities. The underlying mechanisms are complex and largely elusive. Currently, there are several ongoing clinical trials based on the use of activated invariant natural killer T (iNKT) cells.

Bmp2 regulates the interaction between EPDCs and myocytes in cardiac OFT.

Epicardium-derived cells (EPDCs) can migrate into the myocardium, giving rise to several types of cell which are indispensable to compact myocardium and inducing normal myocardial development. Subepicardium accumulates bone morphogenetic proteins (Bmps), which can release into myocardium further. It has been shown that reduced Bmp-mediated signaling in a novel neural crest derivative in the epicardium reduced the cardiomyocyte proliferative activity in the developing myocardium.