KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction

• 영문명: KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Zhihong Chang Hongkun Li
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제27권 제2호, 177~185쪽, 전체 9쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2023.03.31

영문 초록

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.

목차

INTRODUCTION

METHODS

RESULTS

DISCUSSION

FUNDING

ACKNOWLEDGEMENTS

CONFLICTS OF INTEREST

SUPPLEMENTARY MATERIALS

REFERENCES

키워드

Inflammation KLF9 Myocardial infarction Toll-like receptor 2 Transcription factors