References in periodicals archive ?
Here, I propose to investigate the molecular mechanisms that couple mechanical cardiomyocyte strain and cardiomyocyte loss during the heart failure involving the mechanosensing titin filament.
This resulted in extreme cardiomyocyte proliferation and hypertrophy -- excessive growth of the individual cardiomyocytes -- leading to a giant heart (cardiomegaly) that left little room for blood to enter.
Martin's team showed that this was because the specialized heart cells, called cardiomyocytes, were able to proliferate much better: a feat that is essentially lost in normal injured hearts.
Our functional analysis of those genes suggests that homeostatic levels of AHR establish a complex regulatory network that controls various aspects of embryonic development, including cardiomyocyte differentiation.
In addition, the study points to new research directions by suggesting that abnormal cardiomyocyte proliferation may be involved in diseases of the heart muscle (cardiomyopathy) that affect young humans, and that cardiomyocyte proliferation could be stimulated in young humans for the treatment of heart failure.
Heart attacks kill muscle cells called cardiomyocytes, leaving behind tissue damage.
Roche (SIX: RO, ROG; OTCQX: RHHBY) has entered into a collaborative agreement with ChanTest Corporation, a leading ion channel screening provider, to perform cardiac safety testing of potential drug compounds using Roche's xCELLigence System RTCA Cardio Instrument and iCell[R] Cardiomyocytes, human induced pluripotent stem (iPS) cell-derived cardiomyocytes provided by Cellular Dynamics International (CDI).
Fibroblast growth factor has long been known to modulate cardiac morphogenesis and more recently to regulate cardiomyocyte differentiation (Sheikh et al.
Through this collaboration, scientists at Stem Cell Theranostics used Thermo Fisher Scientific workflow reagents to develop stem cell-derived cardiomyocytes from patients with inherited hypertrophic cardiomyopathy (HCM).
The exacerbation of myocardial damage may eventually lead to cardiomyocyte apoptosis and impaired myocardial function.
The progressive decline of cardiomyocyte mitochondrial function is considered a major mechanism underlying heart senescence.
The topics include engineered arterial models to correlate blood flow with the biological response of tissue, umbilical cord blood for cardiovascular cell therapy, heart repair from natural mechanisms of cardiomyocyte production to the design of new cardiac therapies, controversies in blood pressure goal guidelines and masked hypertension, and transcatheter aortic valve implantation and cerebrovascular events.
B-type natriuretic peptide (BNP) [3] is a key regulatory hormone that increases sodium excretion, lowers blood pressure, suppresses the renin-angiotensin-aldosterone system, and inhibits cardiomyocyte hypertrophy and proliferation of cardiac fibroblasts (1-3).
In conclusion, we found that the effects of SHS on cardiomyocyte are mediated by the Fas death-receptor-dependent apoptotic pathway and might be related to the epidemiologic incidence of cardiac disease of SHS-exposed nonsmokers.
Matrix metalloproteinase reduction also may prevent the occurrence of cardiomyocyte apoptosis.