ArticleiScience2025
TRIM13 prevents cardiomyocyte injury by affecting apoptosis through interacting with CD3D in myocardial infarction.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
Myocardial infarction (MI) is a common cardiovascular disease with a high risk of sudden death. We aim to develop potential and more effective therapeutic strategies for treating and preventing MI. A mouse model of MI was established, and cardiac tissue sample microarray data and GSE236374 dataset were collected to screen and 120 upregulation and 15 downregulation genes were obtained, and related to T cells and cell immunity. Further obtained 7 key genes, including Cd8b1, Pdcd1, Klrd1, Klrk1, Cd3g, Cd74, and Cd3d, and had high expression in MI mice. The ceRNA regulation network found that protein TRIM13 was upstream of CD3D.
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