Journal of Inflammation Research (Dec 2023)
Macrophage Heterogeneity and Its Impact on Myocardial Ischemia-Reperfusion Injury: An Integrative Review
Abstract
Shuwan Xu,1,2,* Cong Xu,1,* Jiahua Xu,1 Kun Zhang,2 Huanji Zhang1 1Cardiovascular Department, the Eighth Affiliated Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, People’s Republic of China; 2Department of Cardiology, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Guangzhou, Guangdong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Huanji Zhang, Cardiovascular Department, The Eighth Affiliated Hospital of Sun Yat-Sen University, No. 3025 Shennan Middle Road, Shenzhen, 518033, People’s Republic of China, Tel +8613688808979, Email [email protected] Kun Zhang, Department of Cardiology, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, 107 Yanjiang West Road, Guangzhou, 510120, People’s Republic of China, Tel +8613450390268, Email [email protected]: The coronary reperfusion following acute myocardial infarction can paradoxically trigger myocardial ischemia-reperfusion (IR) injury. This complex phenomenon involves the intricate interplay of different subsets of macrophages. These macrophages are crucial players in the post-infarction inflammatory response and subsequent myocardial anti-inflammatory repair. However, their diverse functions can lead to both beneficial and detrimental effects. On one hand, these macrophages play a crucial role in orchestrating the inflammatory response, aiding in the clearance of cellular debris and initiating tissue repair mechanisms. On the other hand, their excessive infiltration and activation can contribute to the perpetuation of the inflammatory cascade, leading to additional myocardial injury and adverse cardiac remodeling. Multiple mechanisms contribute to the IR injury mediated by macrophages, including oxidative stress, apoptosis, and autophagy. These processes further exacerbate the damage to the already vulnerable myocardial tissue. To address this delicate balance, therapeutic strategies aiming to target and modulate macrophage polarization and function are being explored. By fine-tuning the immune inflammatory response, such interventions hold promise in mitigating post-infarction myocardial injury and fostering a more favorable environment for myocardial healing and recovery. Through advancements in this area of research, potential anti-inflammatory interventions may pave the way for improved clinical outcomes and better management of patients after acute myocardial infarction.Keywords: ischemia-reperfusion injury, macrophages, inflammatory cascade, cardiac remodeling, oxidative stress
