ArticleBritish journal of pharmacology2015
Genistein alleviates pressure overload-induced cardiac dysfunction and interstitial fibrosis in mice.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
- Estrogen signaling processes in fibroblasts: a scoping review.Frontiers in endocrinology · 2026Article
- TGFβ1 accelerated the progression of diabetic nephropathy via up-regulating BRD4/Notch1/YAP signaling induced fibrosis and proliferation in fibroblasts.Scientific reports · 2025Article
- Association of dietary isoflavones intake with all-cause mortality and heart disease mortality: a prospective cohort study.BMC public health · 2025Article
- PD-1 inhibition disrupts collagen homeostasis and aggravates cardiac dysfunction through endothelial-fibroblast crosstalk and EndMT.Frontiers in pharmacology · 2025Article
- Unlocking the Potential: Phytoestrogens and Cardiovascular Health.Current cardiology reviews · 2025Review
- Mechanisms of MTA3 in cancer and related diseases and its clinical applications.Frontiers in oncology · 2025Review
- Genistein inhibits HIF-1α and attenuates high glucose-induced peritoneal mesothelial-mesenchymal transition and fibrosis via the mTOR/OGT pathway.Scientific reports · 2024Article
- Semaphorin‑3A alleviates cardiac hypertrophy by regulating autophagy.Experimental and therapeutic medicine · 2024Article
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect.Journal of cardiovascular development and disease · 2023Review
- Atrazine Toxicity: The Possible Role of Natural Products for Effective Treatment.Plants (Basel, Switzerland) · 2023Review
- Role of polyphenolic compounds and their nanoformulations: a comprehensive review on cross-talk between chronic kidney and cardiovascular diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Phytochemicals as potential target on thioredoxin-interacting protein (TXNIP) for the treatment of cardiovascular diseases.Inflammopharmacology · 2023Review
- Pharmacological Effects of Genistein on Cardiovascular Diseases.Evidence-based complementary and alternative medicine : eCAM · 2023Review
- Small ubiquitin-related modifier (SUMO)ylation of SIRT1 mediates (-)-epicatechin inhibited- differentiation of cardiac fibroblasts into myofibroblasts.Pharmaceutical biology · 2022Article
- Emodin in cardiovascular disease: The role and therapeutic potential.Frontiers in pharmacology · 2022Review
- Advances in the study of emodin: an update on pharmacological properties and mechanistic basis.Chinese medicine · 2021Review
- Current Perspectives on the Beneficial Effects of Soybean Isoflavones and Their Metabolites for Humans.Antioxidants (Basel, Switzerland) · 2021Review
- A nutraceutical strategy for downregulating TGFβ signalling: prospects for prevention of fibrotic disorders, including post-COVID-19 pulmonary fibrosis.Open heart · 2021Article
- Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice.Acta pharmacologica Sinica · 2021Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePressure overload-induced cardiac interstitial fibrosis is viewed as a major cause of heart failure in patients with hypertension or aorta atherosclerosis. The purpose of this study was to investigate the effects and the underlying mechanisms of genistein, a natural phytoestrogen found in soy bean extract, on pressure overload-induced cardiac fibrosis. EXPERIMENTAL APPROACH: Genisten was administered to mice with pressure overload induced by transverse aortic constriction. Eight weeks later, its effects on cardiac dysfunction, hypertrophy and fibrosis were determined. Its effects on proliferation, collagen production and myofibroblast transformation of cardiac fibroblasts (CFs) and the signalling pathways were also assessed in vitro. KEY
resultsPressure overload-induced cardiac dysfunction, hypertrophy and fibrosis were markedly attenuated by genistein. In cultured CFs, genistein inhibited TGFβ1-induced proliferation, collagen production and myofibroblast transformation. Genistein suppressed TGFβ-activated kinase 1 (TAK1) expression and produced anti-fibrotic effects by blocking the TAK1/MKK4/JNK pathway. Further analysis indicated that it up-regulated oestrogen-dependent expression of metastasis-associated gene 3 (MTA3), which was found to be a negative regulator of TAK1. Silencing MTA3 by siRNA, or inhibiting the activity of the MTA3-NuRD complex with trichostatin A, abolished genistein's anti-fibrotic effects. CONCLUSIONS AND IMPLICATIONS: Genistein improved cardiac function and inhibited cardiac fibrosis in response to pressure overload. The underlying mechanism may involve regulation of the MTA3/TAK1/MKK4/JNK signalling pathway. Genistein may have potential as a novel agent for prevention and therapy of cardiac disorders associated with fibrosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.