miR‑26b inhibits isoproterenol‑induced cardiac fibrosis via the Keap1/Nrf2 signaling pathway
- Shaohua Xian
- Jing Li
- Zhengfu Zhang
Affiliations: Department of Cardiothoracic Surgery, The Traditional Chinese Medicine Hospital, Chongqing 408300, P.R. China, Department of Cardiothoracic Surgery, People's Hospital of Changshou, Chongqing 401220, P.R. China
- Published online on: January 15, 2020 https://doi.org/10.3892/etm.2020.8455
Copyright: © Xian
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A critical event in cardiac fibrosis is the transformation of cardiac fibroblasts (CFs) into myofibroblasts. MicroRNAs (miRNAs) have been reported to be critical regulators in the development of cardiac fibrosis. However, the underlying molecular mechanisms of action of miRNA (miR)‑26b in cardiac fibrosis have not yet been extensively studied. In the present study, the expression levels of miR‑26b were downregulated in isoproterenol (ISO)‑treated cardiac tissues and CFs. Moreover, miR‑26b overexpression inhibited the cell viability of ISO‑treated CFs and decreased the protein levels of collagen I and α‑smooth muscle actin (α‑SMA). Furthermore, bioinformatics analysis and dual luciferase reporter assays indicated that Kelch‑like ECH‑associated protein 1 (Keap1) was the target of miR‑26b, and that its expression levels were decreased in miR‑26b‑treated cells. In addition, Keap1 overexpression reversed the inhibitory effects of miR‑26b on ISO‑induced cardiac fibrosis, as demonstrated by cell viability, and the upregulation of collagen I and α‑SMA expression levels. Furthermore, inhibition of Keap1 expression led to the activation of nuclear factor erythroid 2‑related factor 2 (Nrf2), which induced the transcriptional activation of antioxidant/detoxifying proteins in order to protect against cardiac fibrosis. Taken together, the data demonstrated that miR‑26b attenuated ISO‑induced cardiac fibrosis via the Keap‑mediated activation of Nrf2.