Inflammation macrophages contribute to cardiac homeostasis

Author:

Zhang Yu1,Tu Junchu1,Li Yujie1,Wang Yanli1,Lu Lin1,Wu Chengjie1,Yu Xi-yong2,Li Yangxin1

Affiliation:

1. Institute for Cardiovascular Science and Department of Cardiovascular Surgery, First Affiliated Hospital and Medical College of Soochow University, Collaborative Innovation Center of Hematology, Soochow University, Suzhou 215123, China.

2. Key Laboratory of Molecular Target & Clinical Pharmacology and the NMPA & State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou 511436, China.

Abstract

Cardiovascular diseases (CVDs) have high morbidity. Many endogenous and exogenous factors provoke the innate immune response causing tissue damage and accelerating the progression of the diseases. The macrophages are the major cells mediating the inflammatory response. Inflammasomes are multi-protein complexes that recognize danger signals, activate cytokines, and participate in the inflammatory response. Both macrophages and inflammasomes play a critical role in the development and progression of CVDs, such as myocardial infarction, hypertension, and atherosclerosis. This review will summarize the studies on macrophages and inflammasomes and discuss potential therapeutic interventions. Moreover, macrophages and inflammasomes play distinct role in the inflammation process, but closely linked. The inflammasome system occur in macrophages, and macrophage pyroptosis may be provoked by inflammasome activation. The cytokines secreted by macrophages may be related to the activation of inflammasomes, and further activate macrophages in the heart and cause the interconversion of M1 phenotype and M2 phenotype. The mechanism of inflammasomes regulating macrophage polarization remains to be further investigated.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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