ArticleActa pharmacologica Sinica2014
Curcumin attenuates cardiac fibrosis in spontaneously hypertensive rats through PPAR-γ activation.
Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Peroxisome proliferator-activated receptor gamma (PPARγ) as a mechano-metabolic transducer: coordinating lipid homeostasis through mechanical cues.Molecular biomedicine · 2026Review
- The core mechanism of traditional Chinese medicine in improving myocardial fibrosis: restoring the dynamic balance of mitochondrial quality control.Frontiers in cardiovascular medicine · 2026Review
- Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026Review
- Antifibrotic mechanism of curcumin and its therapeutic potential in multi-organ diseases.Frontiers in pharmacology · 2026Review
- The Many Facets of PPAR-γ Agonism in Obesity and Associated Comorbidities: Benefits, Risks, Challenges, and Future Directions.Current obesity reports · 2025Review
- Traditional Chinese medicine compounds modulate signaling pathways to improve cardiac-related pathology.Frontiers in pharmacology · 2025Review
- Exploring the role of curcumin in mitigating oxidative stress to alleviate lipid metabolism disorders.Frontiers in pharmacology · 2025Review
- Review of the Protective Mechanism of Curcumin on Cardiovascular Disease.Drug design, development and therapy · 2024Review
- Antiaging effects of dietary supplements and natural products.Frontiers in pharmacology · 2023Review
- Revealing the Pathogenesis of Salt-Sensitive Hypertension in Dahl Salt-Sensitive Rats through Integrated Multi-Omics Analysis.Metabolites · 2022Article
- Role of curcumin in ameliorating hypertension and associated conditions: a mechanistic insight.Molecular and cellular biochemistry · 2022Review
- The effect of nutraceuticals on multiple signaling pathways in cardiac fibrosis injury and repair.Heart failure reviews · 2022Review
- Impact of Phytochemicals on PPAR Receptors: Implications for Disease Treatments.PPAR research · 2022Review
- Cardiac fibrosis and curcumin: a novel perspective on this natural medicine.Molecular biology reports · 2021Review
- Untangling the Cooperative Role of Nuclear Receptors in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2021Review
- Anti-fibrotic effects of curcumin and some of its analogues in the heart.Heart failure reviews · 2020Review
- Curcumin Attenuates Asthmatic Airway Inflammation and Mucus Hypersecretion Involving a PPARMediators of inflammation · 2019Article
- [Curcumin suppresses cigarette smoke extract-induced oxidative stress through PPARγ/ NF-κB pathway in human bronchial epithelial cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Curcumin suppresses cardiac fibroblasts activities by regulating the proliferation and cell cycle via the inhibition of the p38 MAPK/ERK signaling pathway.Molecular medicine reports · 2018Article
- Peroxisome proliferator-activated receptor-γ and its related pathway in bone marrow mesenchymal stem cell differentiation co-cultured with mechanically stretched ligament fibroblasts.International journal of molecular medicine · 2018Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effects of curcumin (Cur) on cardiac fibrosis in spontaneously hypertensive rats (SHRs) and the mechanisms underlying the anti-fibrotic effect of Cur in rat cardiac fibroblasts (CFs) in vitro.
methodsSHRs were orally treated with Cur (100 mg·kg(-1)·d(-1)) or Cur (100 mg·kg(-1)·d(-1)) plus the PPAR-γ antagonist GW9662 (1 mg·kg(-1)·d(-1)) for 12 weeks. Cultured CFs were treated with angiotensin II (Ang II, 0.1 μmol/L) in vitro. The expression of relevant proteins and mRNAs was analyzed using Western blotting and real-time PCR, respectively. The expression and activity of peroxisome proliferator-activated receptor-γ (PPAR-γ) were detected using Western blotting and a DNA-binding assay, respectively.
resultsTreatment of SHRs with Cur significantly decreased systolic blood pressure, blood Ang II concentration, heart weight/body weight ratio and left ventricle weight/body weight ratio, with concurrently decreased expression of connective tissue growth factor (CTGF), plasminogen activator inhibitor (PAI)-1, collagen III (Col III) and fibronectin (FN), and increased expression and activity of PPAR-γ in the left ventricle. Co-treatment with GW9662 partially abrogated the anti-fibrotic effects of Cur in SHRs. Pretreatment of CFs with Cur (5, 10, 20 μmol/L) dose-dependently inhibited Ang II-induced expression of CTGF, PAI-1, Col III and FN, and increased the expression and binding activity of PPAR-γ. Pretreatment with GW9662 partially reversed anti-fibrotic effects of Cur in vitro. Furthermore, pretreatment of CFs with Cur inhibited Ang II-induced expression of transforming growth factor-β1 (TGF-β1) and phosphorylation of Smad2/3, which were reversed by GW9662.
conclusionCur attenuates cardiac fibrosis in SHRs and inhibits Ang II-induced production of CTGF, PAI-1 and ECM in CFs in vitro. The crosstalk between PPAR-γ and TGF-β1/Smad2/3 signaling is involved in the anti-fibrotic and anti-proliferative effects of Cur.
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