ArticleScientific reports2016
Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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51 citing papers in PubMed, 100 citations in OpenAlex.
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- Chlorogenic acid attenuates cardiac hypertrophy and fibrosis by downregulating galectin 3.Scientific reports · 2025Article
- Antihypertrophic effects of the seed ethanolic extract ofToxicology reports · 2025Article
- Plant Polyphenols as Heart's Best Friends: From Health Properties, to Cellular Effects, to Molecular Mechanisms of Action.International journal of molecular sciences · 2025Review
- Isoproterenol mechanisms in inducing myocardial fibrosis and its application as an experimental model for the evaluation of therapeutic potential of phytochemicals and pharmaceuticals.Animal models and experimental medicine · 2025Review
- Unrevealing the mechanisms behind the cardioprotective effect of wheat polyphenolics.Archives of toxicology · 2024Review
- Exploring in vivo and in vitro models for heart failure with biomarker insights: a review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024Review
- Cardioprotective effect of Vitamin D on cardiac hypertrophy through improvement of mitophagy and apoptosis in an experimental rat model of levothyroxine -induced hyperthyroidism.Molecular biology reports · 2024Article
- Metabolomics analysis reveals the effects ofHeliyon · 2024Article
- Ameliorating impaired cardiac function in myocardial infarction using exosome-loaded gallic-acid-containing polyurethane scaffolds.Bioactive materials · 2024Article
- Gallic Acid Inhibits Proliferation and Migration of Smooth Muscle Cells in a Pig In-Stent Restenosis Model.Chonnam medical journal · 2024Article
- Protective Roles and Therapeutic Effects of Gallic Acid in the Treatment of Cardiovascular Diseases: Current Trends and Future Directions.Current medicinal chemistry · 2024Review
- Protocatechuic acid prevents isoproterenol-induced heart failure in mice by downregulating kynurenine-3-monooxygenase.Journal of cellular and molecular medicine · 2023Article
- Cardioprotective and hypotensive mechanistic insights of hydroethanolic extract ofFrontiers in pharmacology · 2023Article
- Impact of polyphenols on heart failure and cardiac hypertrophy: clinical effects and molecular mechanisms.Frontiers in cardiovascular medicine · 2023Review
- Syringic acid mitigates isoproterenol-induced cardiac hypertrophy and fibrosis by downregulating Ereg.Journal of cellular and molecular medicine · 2022Article
- Yang-xin-xue keli exerts therapeutic effectsFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gallic acid, a type of phenolic acid, has been shown to have beneficial effects in inflammation, vascular calcification, and metabolic diseases. The present study was aimed at determining the effect and regulatory mechanism of gallic acid in cardiac hypertrophy and fibrosis. Cardiac hypertrophy was induced by isoproterenol (ISP) in mice and primary neonatal cardiomyocytes. Gallic acid pretreatment attenuated concentric cardiac hypertrophy. It downregulated the expression of atrial natriuretic peptide, brain natriuretic peptide, and beta-myosin heavy chain in vivo and in vitro. Moreover, it prevented interstitial collagen deposition and expression of fibrosis-associated genes. Upregulation of collagen type I by Smad3 overexpression was observed in cardiac myoblast H9c2 cells but not in cardiac fibroblasts. Gallic acid reduced the DNA binding activity of phosphorylated Smad3 in Smad binding sites of collagen type I promoter in rat cardiac fibroblasts. Furthermore, it decreased the ISP-induced phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal regulated kinase (ERK) protein in mice. JNK2 overexpression reduced collagen type I and Smad3 expression as well as GATA4 expression in H9c2 cells and cardiac fibroblasts. Gallic acid might be a novel therapeutic agent for the prevention of cardiac hypertrophy and fibrosis by regulating the JNK2 and Smad3 signaling pathway.
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