1. Academic Validation
  2. Identification of circulating T-cell immunoglobulin and mucin domain 4 as a potential biomarker for coronary heart disease

Identification of circulating T-cell immunoglobulin and mucin domain 4 as a potential biomarker for coronary heart disease

  • MedComm (2020). 2023 Jul 8;4(4):e320. doi: 10.1002/mco2.320.
Mengyao Wang 1 Ke Gong 1 Xinran Zhu 1 Shasha Chen 1 Jie Zhou 1 Hui Zhang 2 Jihong Han 1 3 Likun Ma 2 Yajun Duan 2
Affiliations

Affiliations

  • 1 Key Laboratory of Metabolism and Regulation for Major Diseases of Anhui Higher Education Institutes, College of Food and Biological Engineering Hefei University of Technology Hefei China.
  • 2 Department of Cardiology The First Affiliated Hospital of USTC Division of Life Sciences and Medicine University of Science and Technology of China Hefei China.
  • 3 Key Laboratory of Bioactive Materials of Ministry of Education College of Life Sciences State Key Laboratory of Medicinal Chemical Biology Nankai University Tianjin China.
Abstract

Efferocytosis, the process of engulfing and removing apoptotic cells, is attenuated in vulnerable plaques of advanced atherosclerosis. T-cell immunoglobulin and Mucin domain 4 (TIMD4) is a recognition receptor protein for efferocytosis that has been implicated in atherosclerosis mouse models. However, the role of serum-soluble TIMD4 (sTIMD4) in coronary heart disease (CHD) remains unknown. In this study, we analyzed serum samples collected from two groups: Group 1 (36 healthy controls and 70 CHD patients) and Group 2 (44 chronic coronary syndrome [CCS]) and 81 acute coronary syndrome [ACS] patients). We found that sTIMD4 levels in patients with CHD were significantly higher than those in healthy controls and were also higher in ACS than in CCS patients. The area under the receiver operating characteristic curve was 0.787. Furthermore, our in vitro results showed that low-density lipoprotein/lipopolysaccharide activated p38 mitogen-activated protein kinase, which in turn enhanced a disintegrin and metalloproteinase 17, resulting in increased secretion of sTIMD4. This impairment of macrophage efferocytosis promoted inflammation. Thus, this study is not only the first identification of a potential novel biomarker of CHD, sTIMD4, but also demonstrated its pathogenesis mechanism, providing a new direction for the diagnosis and treatment of CHD.

Keywords

ADAM17; TIMD4; coronary heart disease; inflammation; p38.

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