High-fat diet exacerbates tac hypertrophy

By | December 17, 2020

high-fat diet exacerbates tac hypertrophy

Further, multiple drugs and proteins protect against the pathological cardiac hypertrophy by inhibiting the p38 MAPK pathway 11, At the end of the study, TAC or Sham operated mice were euthanized and the hearts were rapidly excised and weighed. Nitric oxide synthase modulates angiogenesis in response to tissue ischemia. PLoS One. Deleterious effects of sugar and protective effects of starch on cardiac remodeling, contractile dysfunction, and mortality in response to pressure overload. Wang, S. CD36 KO not only improves the phenotypic response but also normalizes FBG and insulin levels in mice that continue to gain weight. Download citation. We thank Mr.

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Thank you for visiting nature. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. C1q-tumor necrosis factor-related protein-3 CTRP3 is an adipokine, which exerts protective function in ischemic or diabetic heart injury. However, the role of CTRP3 in cardiac hypertrophy remains unclear. The aim of this study was to investigate the pharmacological effects of CTRP3 on pathological cardiac hypertrophy induced by hypertension. After 4 weeks, cardiac hypertrophy, fibrosis, and cardiac function were examined. Compared with WT mice, Ctrp3 deficiency substantially impaired contractile dysfunction, exacerbated the enlargement of cardiomyocytes and myocardial fibrosis, and reprogramed the expression of pathological genes after TAC.

Louis, St. Louis, Missouri, USA. Heart failure HF is the end stage of cardiovascular disease, in which hypertrophic remodeling no longer meets cardiac output demand. Established animal models of HF have provided insights into disease pathogenesis. However, these models are developed on dissimilar metabolic backgrounds from humans — patients with HF are frequently overweight or obese, whereas animal models of HF are typically lean. Thus, we aimed to develop and investigate model for cardiac hypertrophy and failure that also recapitulates the cardiometabolic state of HF in humans.

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