IFI-16 inhibition attenuates myocardial remodeling following myocardial infarction
Yi Deng,
Xiuqing Pang,
Li Chen,
Weihang Peng,
Xiaoyan Huang,
Peiying Huang,
Shuai Zhao,
Zhishang Li,
Xingui Cai,
Qiuping Huang,
Jing Zeng,
Yuchao Feng,
Bojun Chen
Affiliations
Yi Deng
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; The Postdoctoral Research Station, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Xiuqing Pang
Department of Infectious Diseases, the Third Affiliated Hospital of Sun Yat-sen University, 600 Tianhe Road, Guangzhou 510630, China
Li Chen
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Weihang Peng
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Xiaoyan Huang
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Peiying Huang
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Shuai Zhao
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Zhishang Li
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Xingui Cai
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Qiuping Huang
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Jing Zeng
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China
Yuchao Feng
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Corresponding author
Bojun Chen
The Second Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Guangdong Provincial Key Laboratory of Research on Emergency in Traditional Chinese Medicine, Clinical Research Team of Prevention and Treatment of Cardiac Emergencies with Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Emergency Department of Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou City, Guangdong Province 511400, China; Corresponding author
Summary: Myocardial remodeling (MR) following myocardial infarction (MI) contributes to heart failure. Inflammation is a key determinant in cardiac remodeling, with potential prognostic improvements by inhibiting inflammatory factors. Pattern recognition receptors, including interferon gamma-inducible protein-16 (IFI-16), play significant roles in this process, yet its specific involvement remains underexplored. This study investigates IFI-16’s role in initiating inflammation via the inflammasome and its direct interaction with galectin-3 protein post-MI. Elevated IFI-16 levels were observed in human and rat myocytes and a mouse MI model under hypoxic, nutrient-deprived conditions, correlating with increased inflammation-associated proteins. Suppression of IFI-16/IFI-204 using short hairpin RNA (shRNA) lentivirus or adeno-associated virus decreased inflammatory factor activation, thereby mitigating remodeling and enhancing cardiac function post-MI. Co-immunoprecipitation (coIP) and double-fluorescence staining confirmed IFI-16’s ability to interact directly with galectin-3. These findings underscore IFI-16’s critical role as a pro-inflammatory factor in post-MI MR, suggesting its inhibition as a potential therapeutic strategy.
