ArticleMolecular medicine reports2018
Epigallocatechingallate attenuates myocardial injury in a mouse model of heart failure through TGF‑β1/Smad3 signaling pathway.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Running exercise alleviates chronic heart failure by promoting cardiomyocyte autophagic flux through the NEAT1-QKI affecting Beclin1/LC3B mRNA stability.Biology direct · 2026Article
- Evaluation of Neonatal Cardiotoxicity Following Maternal Green Tea Extract Consumption During Pregnancy: An Experimental Rat Study on the Cytochrome c/Caspase-9/Caspase-3 Pathway.Medicina (Kaunas, Lithuania) · 2026Article
- Role of BMP-7 in Cardiovascular Diseases: From Molecular Mechanisms to Therapeutic Horizons.Current drug targets · 2026Review
- Tea consumption and cardiovascular risk and outcomes: mechanistic insights, epidemiological evidence, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
- Cardioprotective Effects of the Natural Antioxidant Epigallocatechin Gallate.Antioxidants (Basel, Switzerland) · 2025Review
- Epigallocatechin Gallate as a Molecular Therapeutic in Heart Failure and Cardio-Oncology: Mechanistic Pathways and Translational Perspectives.International journal of molecular sciences · 2025Review
- Green tea catechins: protectors or threats to DNA? A review of their antigenotoxic and genotoxic effects.Archives of toxicology · 2025Review
- Epigallocatechin-3-gallate therapeutic potential in human diseases: molecular mechanisms and clinical studies.Molecular biomedicine · 2024Review
- MiR-10b-5p attenuates spinal cord injury and alleviates LPS-induced PC12 cells injury by inhibiting TGF-β1 decay and activating TGF-β1/Smad3 pathway through PTBP1.European journal of medical research · 2024Article
- Crosstalk between adipogenesis and aging: role of polyphenols in combating adipogenic-associated aging.Immunity & ageing : I & A · 2024Review
- Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect.Journal of cardiovascular development and disease · 2023Review
- A green tea extract catechin EGCg: Therapeutic potential for pediatric cardiomyopathies.Pediatric discovery · 2023Review
- Effect of Postnatal Epigallocatechin-Gallate Treatment on Cardiac Function in Mice Prenatally Exposed to Alcohol.Antioxidants (Basel, Switzerland) · 2023Article
- SMOC2 plays a role in heart failure via regulating TGF-β1/Smad3 pathway-mediated autophagy.Open medicine (Warsaw, Poland) · 2023Article
- Energy metabolism disorders and potential therapeutic drugs in heart failure.Acta pharmaceutica Sinica. B · 2021Review
- Sodium glucose cotransporter 2 inhibitors: mechanisms of action in heart failure.Heart failure reviews · 2021Review
- Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway.Bioscience reports · 2020Article
- Various aspects of inflammation in heart failure.Heart failure reviews · 2020Review
- MicroRNA-29b-3p Targets SPARC Gene to Protect Cardiocytes against Autophagy and Apoptosis in Hypoxic-Induced H9c2 Cells.Journal of cardiovascular translational research · 2019Article
- Tea Polyphenols in Promotion of Human Health.Nutrients · 2018Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to assess the protective effect of epigallocatechingallate (EGCG) against myocardial injury in a mouse model of heart failure and to determine the mechanism underlying regulation of the transforming growth factor‑β1/mothers against decapentaplegic homolog 3 (TGF‑β1/Smad3) signaling pathway. Mouse models of heart failure were established. Alterations in ejection fraction, left ventricular internal diastolic diameter (LVIDd) and left ventricular internal systolic diameter (LVIDs) were measured by echocardiography. Pathological alterations of myocardial tissue were determined by hematoxylin and eosin, and Masson staining. The levels of serum brain natriuretic peptide (BNP), N‑terminal‑proBNP, interleukin (IL)‑1β, IL‑6, tumor necrosis factor‑α, malondialdehyde, superoxide dismutase and glutathione peroxidase were detected with ELISA. Expression of collagen I, collagen III were detected by western blotting and reverse transcription quantitative polymerase chain reaction. Transforming growth factor‑β1 (TGF‑β1), Smad3, phosphorylated (p)‑Smad3, apoptosis regulator BAX (Bax), caspase‑3 and apoptosis regulator Bcl2 in mouse cardiac tissue were measured by western blotting. P‑smad3 and TGF‑β1 were measured by immunofluorescence staining. EGCG reversed the alterations in LVIDd and LVIDs induced by establishment of the model of heart failure, increased ejection fraction, inhibited myocardial fibrosis, attenuated the oxidative stress, inflammatory and cardiomyocyte apoptosis and lowered the expression levels of collagen I and collagen III. Following treatment with TGF‑β1 inhibitor, the protective effect of EGCG against heart failure was attenuated. The results of the present study demonstrated that EGCG can inhibit the progression and development of heart failure in mice through inhibition of myocardial fibrosis and reduction of ventricular collagen remodeling. This protective effect of EGCG is likely mediated through inhibition of TGF‑β1/smad3 signaling pathway.
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Registered trials
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 OpenQuestion graph.