Through in vitro experiments, the paper investigated whether Lycopene can mitigate cardiac ischemia/reperfusion injury, and further explored underlying mechanism works by inhibiting opening of MPTP.A hypoxia-reoxygenation model was established. CCK8 employed to determine viability H9c2 cardiomyocytes. LDH used degree damage Trypan blue staining applied survival rate Flow cytometry apoptosis Rho...

Repair of the mature mammalian myocardium following injury is impaired by the inability of the majority of cardiomyocytes to undergo cell division. We show that overexpression of the cyclin B1-CDC2 (cell division cycle 2 kinase) complex re-initiates cell division in adult cardiomyocytes. Thus strategies targeting the cyclin B1-CDC2 complex might re-initiate cell division in mature cardiomyocyte...

Reduced activity and expression of endothelial NO synthase (eNOS) is observed in cardiomyocytes from pressure-overloaded hearts with heart failure. The present study was aimed to investigate whether reduced eNOS-derived NO production contributes to the hypertrophic growth and phenotype of these cardiomyocytes. Cultured ventricular cardiomyocytes from adult rats were exposed to Nomega-nitro-l-ar...

Mammalian cardiomyocytes irreversibly lose their capacity to proliferate soon after birth, yet the underlying mechanisms have been unclear. Cyclin D1 and its partner, cyclin-dependent kinase 4 (CDK4), are important for promoting the G1-to-S phase progression via phosphorylation of the retinoblastoma (Rb) protein. Mitogenic stimulation induces hypertrophic cell growth and upregulates expression ...

Cardiomyocytes After Heat Stress To the Editor: It is well-known that prior in vivo heat stress induces the synthesis of heat shock protein (HSP) 72 in the rat heart, but the precise content in the various cell-types has not yet been measured. It is therefore of great importance to conduct experiments as performed in the paper by Leger et al.1 However, the overall conclusion that heat pretreatm...

Abstract Pathological cardiac hypertrophy is a leading cause of heart failure, but knowledge the full repertoire cells and their gene expression profiles in human hypertrophic missing. Here, by using large-scale single-nucleus transcriptomics, we present transcriptional response cardiomyocytes to pressure overload caused aortic valve stenosis describe major alterations cellular crosstalk. Hyper...

Human myocardium has long been considered to have essentially no intrinsic regenerative capacity. Recent studies in rodent models, however, have suggested the presence of an extracardiac stem cell population, perhaps in bone marrow, that is capable of some reconstitution of cardiomyocytes after injury. To determine whether similar mechanisms exist in the human heart, we evaluated human female a...

Volume regulatory Cl- channels are key regulators of ischemic preconditioning (IPC). Because Cl- efflux must be balanced by an efflux of cations to maintain cell membrane electroneutrality during volume regulation, we hypothesize that I(K1) channels may play a role in IPC. We subjected cultured cardiomyocytes to 60-minute simulated ischemia (SI) followed by 60-minute of simulated reperfusion (S...

A heart attack kills off many cells in the heart. Parts of the heart become thin and fail to contract properly following the replacement of lost cells by scar tissue. However, the notion that the same adult cardiomyocytes beat throughout the lifespan of the organ and organism, without the need for a minimum turnover, gives way to a fascinating investigations. Since the late 1800s, scientists an...

Reactive oxygen species (ros)-producing nadph oxidases have been shown to play an important role under different (patho)physiological conditions. Especially nox1, nox2 and nox4 have been proven as important sources of ros in the heart. Knowledge of the calcium-dependent nox5 in the heart is lacking. The presence of nox5 was studied via rt-pcr in heart tissue from end-stage heart failure patient...