ArticleCardiovascular drugs and therapy2026
Crocetin Attenuates Fibroblast-to-Myofibroblast Transition after Myocardial Infarction in Mice by Regulating Autophagy.
Article in Cardiovascular drugs and therapy, 2026. 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.
- Shenfu Injection Inhibits Cardiac Fibroblast Activation and Improves Myocardial Fibrosis by Down-regulating M1 Macrophage-Derived Exosomal miR-155-5p.Cardiovascular drugs and therapy · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
purposeMyocardial infarction (MI) triggers pathological remodeling characterized by fibrosis and subsequent fibroblast-to-myofibroblast transition (FMT). Autophagy exerts a dual role in cardiac repair, balancing protective and detrimental effects. Crocetin, a carotenoid derived from saffron, exhibits anti-inflammatory and cardioprotective properties; however, its influence on autophagy-related FMT following MI remains unclear.This study aims to determine whether crocetin mitigates post-MI fibrosis and FMT by modulating autophagy in cardiac fibroblasts (CFs), while also evaluating its effects on cardiac function, infarct size, and autophagic flux.
methodsIn vivo: Mice subjected to MI were administered crocetin (25-100 mg/kg). Cardiac function was assessed via echocardiography, and fibrosis was evaluated through Masson's trichrome staining and immunofluorescence analysis for α-SMA/LC3. In vitro: Hypoxic CFs were treated with crocetin or the autophagy inhibitor 3-methyladenine (3-MA). The effects on autophagic flux (GFP-RFP-LC3), protein expression (Beclin-1, LC3-II/I, P62), and mitochondrial membrane potential (JC-1) were analyzed.
resultsCrocetin enhanced cardiac function, and reduced infarct size and fibrosis in a dose-dependent manner, while suppressing α-SMA expression. It promoted autophagic flux (as evidenced by increased LC3-II levels and autolysosome formation) and mitophagy (indicated by decreased mitochondrial membrane potential). Treatment with 3-MA negated the antifibrotic effects of crocetin.
conclusionCrocetin attenuates post-MI pathological remodeling by enhancing autophagic flux to inhibit FMT, thereby identifying it as a promising candidate for antifibrotic therapy.
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