MicroRNA‑146a attenuates isoproterenol‑induced cardiac fibrosis by inhibiting FGF2
- Hongliang Zhang
- Huijuan Wen
- Yang Huang
Affiliations: Department of Emergency, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China, Department of Gerontology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China
- Published online on: June 9, 2022 https://doi.org/10.3892/etm.2022.11433
Copyright: © Zhang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Cardiac fibrosis is a key factor of heart failure. Increasing evidence suggests that microRNAs (miRNAs/miRs) serve vital roles in the pathogenesis of cardiac fibrosis. The present study aimed to investigate the role of miR‑146a‑5p in isoproterenol (ISO)‑induced cardiac fibrosis. Reverse transcription‑quantitative PCR analysis demonstrated that miR‑146a‑5p expression was downregulated in ISO‑treated rat heart tissue and ISO‑induced cardiac fibroblasts (CFs). Conversely, the expression levels of basic fibroblast growth factor 2 (FGF2), collagen I and smooth muscle α‑actin (α‑SMA) were upregulated in ISO‑treated rat cardiac tissue and CFs. Furthermore, viability and differentiation were inhibited in ISO‑induced CFs transfected with miR‑146a‑5p mimics. Dual‑luciferase reporter assay confirmed that miR‑146a‑5p targeted FGF2. Notably, FGF2 expression was suppressed following overexpression of miR‑146a‑5p, while FGF2 expression increased following miR‑146a‑5p knockdown. In addition, FGF2 knockdown suppressed the expression levels of FGF2, collagen I and α‑SMA levels in CFs. Taken together, the results of the present study suggested that the miR‑146a‑5p/FGF2 pathway may be a novel therapy for cardiac fibrosis.