ArticleCardiovascular diagnosis and therapy2022
Triggering receptor expressed on myeloid cells-2 promotes survival of cardiomyocytes after myocardial ischemic injury through PI3K/AKT pathway.
Article in Cardiovascular diagnosis and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs.Frontiers in immunology · 2026Review
- Integrative single-cell and spatial transcriptome analysis reveals the functions of TREM2Molecular and cellular biochemistry · 2025Article
- Image-Derived Blood Normalization of Antibody-Based TREM2 PET in Mouse Models of Amyloidosis and Myocardial Infarction.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- TREM2 as a regulator of obesity-induced cardiac remodeling: mechanisms and therapeutic insights.American journal of physiology. Heart and circulatory physiology · 2025Review
- The various roles of TREM2 in cardiovascular disease.Frontiers in immunology · 2025Review
- The Protective Role of TREM2 in the Heterogenous Population of Macrophages during Post-Myocardial Infarction Inflammation.International journal of molecular sciences · 2023Review
- The Strategies for Treating "Alzheimer's Disease": Insulin Signaling May Be a Feasible Target.Current issues in molecular biology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous studies have already revealed that triggering receptor expressed on myeloid cells-2 (TREM2) plays a significant protective role during the pathogenesis of ischemia injury in both brain and liver. This study aims to investigate the effect of TREM2 in myocardial ischemic injury. Methods: The mice myocardial infarction (MI) model was established via left anterior descending coronary artery ligation. TREM2 expression was examined with RT-PCR and Western blot. Whereafter, mice were randomly divided into control, sham, MI, Ad.TREM2 transfection group and Ad.Null transfection group. Recombinant adenovirus containing the gene coding full-length mouse TREM2 and EGFP (Ad.TREM2) or control vector containing Results: Compared with the sham group, TREM2 expression was significantly up-regulated in cardiac tissue in mice with MI. Cardiac tissue in mice transfected with Ad.TREM2 was demonstrated with alleviated injury, reduced infarct size, and decreased number of apoptotic cells. Echocardiography revealed that heart function was significantly improved in Ad.TREM2 transfection mice. Also, TREM2 transfection significantly activated the phosphorylation of AKT. At last, the plasma concentration of TREM2 was significantly elevated in patients with CAD and correlated with the severity of CAD. Conclusions: TREM2 may curb myocardial ischemia injury via activating PI3K/AKT signal pathway. Besides, plasma TREM2 may be treated as a potential biomarker in the diagnosis of CAD to reflect the severity of coronary stenosis.
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