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Updated: Jun 11, 2025

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
KLF6 aggravates myocardial fibrosis by promoting mitochondrial division
Tingting Zhang1, Hongyao Ge2, Qiuhang Song3
1Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, China / Department of Biochemistry and Molecular Biology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education of China, Hebei Medical University, Shijiazhuang, Hebei, China.
Abstract:
The dysregulation of mitochondrial dynamics in cardiac fibroblasts (CFs) is closely linked to myocardial fibrosis, which can induce cardiac dysfunction and even lead to heart failure. As an essential multifunctional zinc-finger transcriptional factor of cardiovascular remodeling, the role of KLF6 mediating the link between mitochondrial fission and myocardial fibrosis remains unclear. Next, we want to explore whether the effect of KLF6 on mitochondrial fission might influence cardiac fibroblasts, we established a model of Transforming growth factor β1 (TGF-β1) and Isoprenaline (ISO)-induced myocardial fibrosis. Here, we found that KLF6 up-regulation in CFs is correlated with myocardial fibrosis. While knockdown of KLF6 suppresses mitochondrial fission and the Keap1/Nrf2 pathway molecules, which alleviates myocardial fibrosis induced by TGF-β1. Our findings not only clarified the regulation mechanism of mitochondrial fission by KLF6 but also provided a potential therapeutic target for cardiovascular disease.
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