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One of the key effectors of morphological changes in the hypertensive heart has been demonstrated by myocyte enhancer factor 2, which is part of a complex network of molecular signaling regulating cardiac gene expression. Multiple pathological mechanisms that lead to debilitating cardiac hypertrophy and ultimately heart failure in mammalian heart research can be activated by chronic pressure pressure-overload models that mimic hypertension in the mammalian heart.
Source link: https://europepmc.org/article/MED/35026393
Heart failure with hypertension-mediated cardiac disease with left ventricular hypertrophy and heart failure remain difficult. We've figured carboxypeptide X 2 as a genetic locus affecting LV mass here. In Cpxm2-deficient and wild-type mice exposed to deoxycorticosterone acetate acetate, the functional role of Cpxm2 was further investigated. WT mice suffered severe LV loss, including increases in LV masses and diameters, impairment of LV systolic and diastolic function, and reduced ejection percentages. CPXM2 expression was found to have a significant increase in endomyocardial biopsies from patients with cardiac hypertrophy.
Source link: https://europepmc.org/article/MED/34916661
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