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Cardiac Hypertrophy Heart Failure - Europe PMC

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Last Updated: 13 August 2022

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Na + /H + Exchanger 1, a Potential Therapeutic Drug Target for Cardiac Hypertrophy and Heart Failure.

Cardiac hypertrophy is defined as an elevated heart mass in reaction to higher hemodynamic demands. The incidence of heart failure is due to myocardial infarction, which could be salvaged by reperfusion and eventually leads to a fatal myocardial ischemia-reperfusion injury. Na + / H + exchangers are membrane transporters that convert one intracellular proton into one extracellular Na +. NHE1 catalyzes increased intracellular Na + levels during myocardial hypotension, leading to Ca 2+ overload and subsequent myocardial injury.

Source link: https://europepmc.org/article/MED/35890170


Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure.

Blood pressure can contribute to atherosclerotic plaque formation by acting as a physical force that helps expedite the migration of pro-atherogenic lipoproteins across the endothelium. Mouse deficient mice of C57BL/6N have elevated remnant lipoproteins, which are a risk factor for coronary atherosclerosis. Following transverse aortic constriction in C57BL/6N E -/- mice, we wanted to determine the effects of increased remnant lipoproteins on the formation of pressure overload-induced cardiac hypertrophy and heart failure in this research. C57BL/6N TAC mice's left coronary artery was found in the left coronary artery, but not in C57BL/6N TAC mice. In C57BL/6N TAC mice, pressure overload resulted in markedly elevated cardiac hypertrophy and more pronounced heart failure.

Source link: https://europepmc.org/article/MED/35884897


Angiotensin receptor-neprilysin inhibitor attenuates cardiac hypertrophy and improves diastolic dysfunction in a mouse model of heart failure with preserved ejection fraction.

We investigated the effect of LCZ696 on HFpEF in transverse aortic constriction mice and compared it to the angiotensin receptor blocker, valsartan. In mice with overload-induced diastolic dysfunction, LCZ696 improved cardiac diastolic function by reducing ventricular hypertrophy and fibrosis. LCZ696 is a potent suppressor of activated T cells signal transduction pathways, and as a potential root mechanism.

Source link: https://europepmc.org/article/MED/35596518


CCL17 acts as a novel therapeutic target in pathological cardiac hypertrophy and heart failure.

The prevalence of an age-stratified healthy population and a younger community-based cohort, as well as heart failure patients' study, showed that the prevalent C-C motif ligand 17 level increased with age and was strongly associated with cardiac dysfunction. We discover that chemokine CCL17 is a novel therapeutic target in age-related and Ang II-induced pathological cardiac hypertrophy and heart failure.

Source link: https://europepmc.org/article/MED/35687056


Cullin-associated and neddylation-dissociated 1 protein (CAND1) governs cardiac hypertrophy and heart failure partially through regulating calcineurin degradation.

Pathological cardiac hypertrophy is a process that is characterized by significant protein turnover disruption. Following substrate accumulation, a coordinator to modulate substrate protein degradation, as a mediator to reduce substrate protein degradation by encouraging the synthesis of specific cullin-based ubiquitin ligase 3 complex, which may also aid in the maintenance of normal protein homeostasis. We should therefore investigate the role of CAND1 in cardiac hypertrophy and heart failure as well as the underlying molecular mechanism. We found that the CAND1 protein level in cardiac tissues from heart failure patients and TAC mice had increased in heart failure patients and TAC mice, whereas the mRNA level did not change. CAND1 overexpression at the molecular level was downregulated, but CAND1-KO+/- or knockdown upregulated calcineurin expression both in vivo and vitro conditions. Notably, CAND1's deficiency-induced hypertrophic phenotypes were partially salvaged by calcineurin's downturn, but exogenous CAND1 inhibited TAC-induced cardiac hypertrophy.

Source link: https://europepmc.org/article/MED/35661710

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions