Key result
Circulating miR-21 levels were significantly higher in patients with hypertensive heart disease compared to controls and positively correlated with serum myocardial fibrotic markers.
Why the study?
Hypertension causes cardiac remodeling leading to hypertensive heart disease, but the contribution of microRNA-21 to cardiac remodeling in hypertension is poorly understood.
Observational (n=20)
No
p-value: p=<0.05
Suppression of miR-21 prevents hypertension-induced cardiac remodeling by regulating the PDCD4, AP-1, and TGF-β1 signaling pathway, identifying a potential therapeutic target for hypertensive heart disease.
Elevated miR-21 may indicate fibrosis in hypertensive heart disease; animal data leave open therapeutic targeting.
Hypertension is a major public health problem among the aging population worldwide. It causes cardiac remodeling, including hypertrophy and interstitial fibrosis, which leads to development of hypertensive heart disease (HHD). Although microRNA-21 (miR-21) is associated with fibrogenesis in multiple organs, its contribution to cardiac remodeling in hypertension is poorly understood. Circulating miR-21 level was higher in patients with HHD than that in the control subjects. It also positively correlated with serum myocardial fibrotic markers. MiR-21 expression levels were significantly upregulated in the mice hearts after angiotensin II (Ang II) infusion or transverse aortic constriction (TAC) compared with control mice. Expression level of programmed cell death 4 (PDCD4), a main target of miR-21, was significantly decreased in Ang II infused mice and TAC mice compared with control mice. Expression levels of transcriptional activator protein 1 (AP-1) and transforming growth factor-β1 (TGF-β1), which were downstream targets of PDCD4, were increased in Ang II infused mice and TAC mice compared with control mice. In vitro, mirVana-miR-21-specific inhibitor attenuated Ang II-induced PDCD4 downregulation and contributed to subsequent deactivation of AP-1/TGF-β1 signaling pathway in neonatal rat cardiomyocytes. Thus, suppression of miR-21 prevents hypertrophic stimulation-induced cardiac remodeling by regulating PDCD4, AP-1, and TGF-β1 signaling pathway.
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Watanabe et al. (2020) conducted an observational in Hypertensive heart disease (n=20). Hypertensive heart disease vs. Control subjects with normal cardiac function was evaluated on Circulating miR-21 levels and correlation with serum myocardial fibrotic markers (p=<0.05). Circulating miR-21 levels were significantly higher in patients with hypertensive heart disease compared to controls and positively correlated with serum myocardial fibrotic markers.
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