Korean J Physiol Pharmacol 2023; 27(2): 177-185
Published online March 1, 2023 https://doi.org/10.4196/kjpp.2023.27.2.177
Copyright © Korean J Physiol Pharmacol.
Zhihong Chang and Hongkun Li*
Department of Cardiology, Heji Hospital of Changzhi Medical College, Changzhi 046011, China
Correspondence to:Hongkun Li
Author contributions: Z.C. performed the experiments, and collected and analyzed the data. H.L. conceived and designed the experiments.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
The excessive inflammatory response induced by myocardial infarction exacerbates heart injury and leads to the development of heart failure. Recent studies have confirmed the involvement of multiple transcription factors in the modulation of cardiovascular disease processes. However, the role of KLF9 in the inflammatory response induced by cardiovascular diseases including myocardial infarction remains unclear. Here, we found that the expression of KLF9 significantly increased during myocardial infarction. Besides, we also detected high expression of KLF9 in infiltrated macrophages after myocardial infarction. Our functional studies revealed that KLF9 deficiency prevented cardiac function and adverse cardiac remodeling. Furthermore, the downregulation of KLF9 inhibited the activation of NF-κB and MAPK signaling, leading to the suppression of inflammatory responses of macrophages triggered by myocardial infarction. Mechanistically, KLF9 was directly bound to the TLR2 promoter to enhance its expression, subsequently promoting the activation of inflammation-related signaling pathways. Our results suggested that KLF9 is a pro-inflammatory transcription factor in macrophages and targeting KLF9 may be a novel therapeutic strategy for ischemic heart disease.
Keywords: Inflammation, KLF9, Myocardial infarction, Toll-like receptor 2, Transcription factors
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