ArticleCardiovascular diagnosis and therapy2025
Apolipoprotein M delays the development of atherosclerosis by regulating autophagy and mitochondrial function.
Article in Cardiovascular diagnosis and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Current status and challenges of multi-omics research using animal models of atherosclerosis.Journal of molecular and cellular cardiology plus · 2025Review
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11 authors.
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Abstract
Background: Apolipoprotein M (ApoM), a protein component of lipoproteins, is closely related to the development of atherosclerosis, but the specific mechanism remains elusive. Mitochondrial DNA damage can contribute to atherosclerosis, so this study was designed to investigate whether ApoM influences the structure and function of mitochondria during the progression of atherosclerosis and to explore the underlying mechanism. Methods: Atherosclerosis models were established in male ApoM-deficient ( Results: In Conclusions: ApoM exerts atheroprotective effects by promoting autophagy and regulating mitochondrial dynamics, thereby maintaining mitochondrial integrity and function. This study provides novel insights into the mechanisms underlying the protective role of ApoM in atherosclerosis and highlights its potential as a therapeutic target for cardiovascular diseases.
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