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REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1462508
This article is part of the Research Topic Immunity, Atherosclerosis and Cardiovascular Disease: An Interdisciplinary Approach to Cardiometabolic Health View all 7 articles
The various roles of TREM2 in cardiovascular disease
Provisionally accepted- Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha, China
Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane immune receptor that is expressed mainly on macrophages. As a pathology-induced immune signaling hub, TREM2 senses tissue damage and activates immune remodeling in response. Previous studies have predominantly focused on the TREM2 signaling pathway in Alzheimer's disease, metabolic syndrome, and cancer. Recent research has indicated that TREM2 signaling is also activated in various cardiovascular diseases. In this review, we summarize the current understanding and the unanswered questions regarding the role of TREM2 signaling in mediating the metabolism and function of macrophages in atherosclerosis and various models of heart failure.In the context of atherosclerosis, TREM2 signaling promotes foam cell formation and is crucial for maintaining macrophage survival and plaque stability through efferocytosis and cholesterol efflux. Recent studies on myocardial infarction, sepsis-induced cardiomyopathy, and hypertensive heart failure also implicated the protective role of TREM2 signaling in cardiac macrophages through efferocytosis and paracrine functions. Additionally, we discuss the clinical significance of elevated soluble TREM2 (sTREM2) in cardiovascular disease and propose potential therapies targeting TREM2. The overall aim of this review is to highlight the various roles of TREM2 in cardiovascular diseases and to provide a framework for therapeutic strategies targeting TREM2.
Keywords: macrophage, TREM2, Atherosclerosis, Myocardial Infarction, Sepsis-induced cardiomyopathy, HFpEF (Min.5-Max. 8
Received: 10 Jul 2024; Accepted: 10 Feb 2025.
Copyright: © 2025 Wang, Chenghui and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Shuai Wang, Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha, China
Daoquan Peng, Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha, China
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