ArticleFrontiers in pharmacology2025
Chlorogenic acid modulates mitochondrial damage and mitophagy to repair injured myocardial tissue and cells.
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 3 papers.
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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
3 citing papers in PubMed.
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Article
- Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.Frontiers in pharmacology · 2026Article
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Authors and funding
3 authors.
Funding
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Abstract
Background: Chlorogenic acid (CGA) is a polyphenolic compound widely present in plants. It is primarily extracted from the leaves of Eucommia ulmoides, a native medicinal herb. Purpose: This study aimed to investigate the cardioprotective effects of CGA on myocardial infarction (MI) by modulating mitochondrial damage and mitophagy through the PINK1/Parkin signaling pathway. Methods: Results: CGA significantly improved cell viability and reduced oxidative stress in H9C2 cells. It also stabilized mitochondrial membrane potential, increased ATP levels, upregulated PINK1/Parkin expression and increase autophagy flux, Lysosomal inhibitor treatment elevates expression of Parkin, P62 and LC3-II. In MI rats, CGA reduced ROS levels, improved myocardial tissue integrity, reduced fibrosis, and enhanced cardiac function. Detected by electron microscopy, immunohistochemistry, and WB confirmed increased mitophagy in CGA-treated rats. Metabolomics analysis revealed significant alterations in metabolic pathways, particularly related to organic acids and amino acid metabolism. Conclusion: This study demonstrates that CGA exerts cardioprotective effects by modulating mitochondrial damage and promoting mitophagy through the PINK1/Parkin pathway. Our findings provide new insights into the therapeutic potential of CGA for MI treatment and suggest a promising natural compound for myocardial protection.
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