Therapeutic Modulation of Mitophagy by Cafestol in Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis
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Le résumé fourni par la source
Background/Objectives: Mitophagy, the selective removal of damaged mitochondria, plays a pivotal role in regulating cardiac hypertrophy and fibrosis under pressure overload. Targeting mitophagy may help mitigate adverse cardiac remodeling. This preclinical study examined the effects of cafestol, a coffee-derived diterpene, on pressure overload-induced cardiac hypertrophy and fibrosis in mice, with emphasis on mitophagy modulation and mitochondrial ultrastructure. Methods: Male normotensive mice underwent transverse aortic constriction (TAC) and received cafestol at 2, 10, or 50 mg/kg/day via oral gavage for 28 days. Cardiac function was assessed by echocardiography. Histological and molecular analyses quantified fibrosis, inflammation, and apoptosis. Protein expression of CD68, CTGF, DDR2, α-SMA, CD44, galectin-3 (Gal3), collagen I, GAPDH, Bcl-2, Bax, cleaved caspase-3, GRP78, p-ERK/ERK, ATF4, p-mTOR/mTOR, and p62 was evaluated. Transmission electron microscopy (TEM) was used to assess autophagosome formation and mitochondrial morphology. Results: TAC induced significant cardiac hypertrophy and fibrosis, accompanied by elevated expression of fibrotic (CTGF, DDR2, α-SMA, collagen I), inflammatory (CD68, CD44, Gal3), apoptotic (Bax, cleaved caspase-3), and endoplasmic reticulum stress markers (GRP78, ATF4). TEM revealed increased autophagosome accumulation and disrupted mitochondrial architecture. Cafestol treatment reduced collagen deposition, immune cell infiltration, and apoptotic signaling; enhanced Bcl-2 expression; and restored p62 levels. TEM findings demonstrated decreased autophagosome burden and preserved mitochondrial structure, consistent with improved mitophagic flux and mitochondrial homeostasis. Conclusions: Cafestol mitigated pressure overload-induced cardiac remodeling in mice by modulating mitophagy, suppressing fibrotic and inflammatory responses, and preserving mitochondrial integrity. These findings support further investigation of cafestol’s mechanisms and safety profile in preclinical models of cardiovascular disease.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Therapeutic Modulation of Mitophagy by Cafestol in Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis
- Date Crossref
- 25/11/2025
- Éditeur
- MDPI AG
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Ministry of Health and Welfare pays non établi dans la noticeOrganisme public
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Taipei Medical University Department of Internal Medicine pays non établi dans la noticeUniversité ou école supérieure
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Taipei Medical University-Shuang Ho Hospital pays non établi dans la noticeÉtablissement de santé
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Taipei Municipal YangMing Hospital pays non établi dans la noticeÉtablissement de santé
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Institute of Biomedical Sciences pays non établi dans la noticeStructure de recherche
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China Medical University Department of Internal Medicine and Graduate Institute of Clinical Medical Science pays non établi dans la noticeUniversité ou école supérieure
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School of Medicine Department of Internal Medicine pays non établi dans la noticeUniversité ou école supérieure
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Taipei Municipal Chenggong High School pays non établi dans la noticeOrganisation à but non lucratif
Ministry of Health and Welfare, Department of Internal Medicine — Taipei Medical University et Taipei Medical University-Shuang Ho Hospital, avec 5 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.