Authors
Jiwei Gu, Yanjia Wang, Jingru Xu, Xinyi Li, Jieping Zhang, Zhen Li, Xi Xu, Kaiyue Qin, Yajuan Fu, Qianqian Wu, Anning Yang, Xiaohan Li, Xiaoling Yang
Published in
Acta biochimica et biophysica Sinica. Jan 25, 2026. Epub Jan 25, 2026.
Abstract
Pressure overload-induced cardiac hypertrophy and myocardial fibrosis constitute key pathological substrates of heart failure and arrhythmias. This study investigates the protective effects of pterostilbene, a natural small-molecule phenolic compound, against angiotensin II (Ang II)-induced myocardial hypertrophy and fibrosis, and elucidates the underlying mechanisms. Eighteen C57BL/6J mice are randomly allocated into control, Ang II model, and pterostilbene treatment groups. Echocardiographic assessment demonstrates that compared with controls, Ang II administration significantly increases the heart weight-to-body weight ratio and impairs cardiac function. Histopathological analysis reveals pronounced myocardial fibrosis in the model group, accompanied by elevated expression of Collagen I and Collagen III. Notably, pterostilbene treatment significantly attenuates cardiac hypertrophy, improves cardiac function, and ameliorates myocardial fibrosis. Mechanistically, Ang II stimulation markedly downregulates miR-138-5p expression, whereas oxidative stress-induced growth inhibitor 1 (OSGIN1) is identified as its direct target. Pterostilbene upregulates miR-138-5p and downregulates OSGIN1expression within myocardial tissue. Furthermore, serum hydroxyproline levels are significantly elevated in Ang II-treated mice but are reduced following pterostilbene administration. In vitro assays further confirm that pterostilbene alleviates Ang II-induced cardiomyocyte hypertrophy and fibrosis concomitant with increased miR-138-5p expression. Dual-luciferase reporter assays confirmed the direct binding between miR-138-5p and OSGIN1, and OSGIN1 knockdown further enhanced the anti-hypertrophic effects of pterostilbene. Collectively, these findings demonstrate that pterostilbene effectively ameliorates Ang II-induced myocardial hypertrophy and fibrosis, potentially via the upregulation of miR-138-5p, highlighting its therapeutic potential for heart failure and arrhythmias.
PMID:
42634870
Bibliographic data and abstract were imported from PubMed on 24 Aug 2026.
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