ArticleFrontiers in pharmacology2025
The potential mechanism of celastrol attenuating atherosclerosis by promoting macrophage autophagy via AMPK/ULK1 pathway.
Article in Frontiers in pharmacology, 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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Natural Products Modulate Plaque Macrophage Functional Programs in Atherosclerosis.Drug design, development and therapy · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Background: This study aimed to elucidate the molecular mechanisms by which celastrol (Cel) alleviates atherosclerosis (AS) through the regulation of macrophage autophagy. Methods: An AS model was established using ApoE Results: Cel markedly reduced aortic plaque formation, ameliorated dyslipidemia, attenuated inflammatory responses, and enhanced plaque stability in ApoE Conclusion: Cel exerts anti-atherosclerotic effects by activating macrophage autophagy via the AMPK/ULK1 pathway, thereby improving lipid metabolism, reducing inflammation, and stabilizing plaques. These findings highlight the therapeutic potential of Cel and provide new insights into autophagy-targeted strategies against AS.
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Registered trials
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