Protective Effects of SIRT2 Inhibition on Cardiac Fibrosis.
Abstract
A primary factor in the pathogenesis of aging is oxidative stress, with cardiac inflammation and fibrosis being contributed to by increased oxidative stress as organisms age. Oxidative stress enhances the cardiac fibrotic signaling pathway, with reactive oxygen species inducing cardiac fibrosis through increased expression of the profibrotic factor transforming growth factor-beta 1 (TGF-β1). Furthermore, Wnt/β-catenin signaling pathway is implicated in interstitial fibrosis, which is associated with TGF-β. Sirtuin 2 (SIRT2) is expressed in heart tissue, with protective effects in pathological cardiac hypertrophy. We aimed to investigate the mechanisms of cardiac fibrosis in D-Galactose (D-Gal)-induced accelerated aging, focusing on TGF-β1, β-catenin, and SIRT2.
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Research summary
The paper investigates the protective effects of SIRT2 inhibition on cardiac fibrosis, linking oxidative stress and fibrotic signaling pathways to aging. This research is relevant as it addresses mechanisms underlying cardiac fibrosis, which is a significant age-related condition, potentially contributing to our understanding of aging processes.
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