ArticleJournal of cellular and molecular medicine2019
Sodium butyrate attenuates angiotensin II-induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6-dependent mechanism.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 90 citations in OpenAlex.
- Acetyl-CoA synthetase 2 maintains cytosolic acetyl-CoA homeostasis to preserve mitochondrial integrity and attenuate cardiac dysfunction under chronic β-adrenergic stress.Journal of molecular and cellular cardiology plus · 2026Article
- Butyrate and Butyrate-Producing Bacteria in Cardiovascular-Kidney-Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2026Review
- Microbiome-Associated Drug Response Variability in Heart Failure Treatment.Life (Basel, Switzerland) · 2026Review
- Sodium Butyrate Attenuates Isoprenaline-Induced Myocardial Injury via Restoring the Gut-Heart Axis and Suppressing TLR4/NF-κB Signaling.Current issues in molecular biology · 2026Article
- Roflumilast Enhances Liraglutide's Atrial Natriuretic Peptide-Dependent Suppression of Adrenal Aldosterone Secretion.International journal of molecular sciences · 2026Article
- Gut Microbiota and Short-Chain Fatty Acids in Cardiometabolic HFpEF: Mechanistic Pathways and Nutritional Therapeutic Perspectives.Nutrients · 2026Review
- The role of Western diet and gut microbiota in the pathogenesis of cardiovascular diseases.Frontiers in microbiology · 2026Review
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
- Contribution of histone deacetylases (HDACs) to the regulation of histone and non-histone proteins: implications for fibrotic diseases.BMB reports · 2025Review
- HDACs and Their Inhibitors on Post-Translational Modifications: The Regulation of Cardiovascular Disease.Cells · 2025Review
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Role of Gut Microbial Metabolites in Ischemic and Non-Ischemic Heart Failure.International journal of molecular sciences · 2025Review
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- Janus Kinase 2/Signal Transducer and Activator of Transcription 3/Cyclooxygenase 2 Signaling Pathway Mediates the Effect of Central Angiotensin II on the Elevation of Rostral Ventrolateral Medulla Prostaglandin EJournal of the American Heart Association · 2025Article
- Sodium Butyrate, A Gut Microbiota Derived Metabolite in Type 2 Diabetes Mellitus and Cardiovascular Disease: A Review.Cardiovascular & hematological agents in medicinal chemistry · 2025Review
- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- The Role of Short-Chain Fatty Acids in Myocardial Ischemia-Reperfusion Injury.Current nutrition reports · 2024Review
- Low-Molecular-Weight Compounds Produced by the Intestinal Microbiota and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Histone deacetylase 6 controls cardiac fibrosis and remodelling through the modulation of TGF-β1/Smad2/3 signalling in post-infarction mice.Journal of cellular and molecular medicine · 2024Article
- The Human Microbiome-A Physiologic Perspective.Comprehensive Physiology · 2024Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium butyrate (NaBu) is reported to play important roles in a number of chronic diseases. The present work is aimed to investigate the effect of NaBu on angiotensin II (Ang II)-induced cardiac hypertrophy and the underlying mechanism in in vivo and in vitro models. Sprague Dawley rats were infused with vehicle or Ang II (200 ng/kg/min) and orally administrated with or without NaBu (1 g/kg/d) for two weeks. Cardiac hypertrophy parameters and COX2/PGE2 pathway were analysed by real-time PCR, ELISA, immunostaining and Western blot. The cardiomyocytes H9C2 cells were used as in vitro model to investigate the role of NaBu (2 mmol/L) in inhibition of Ang II-induced cardiac hypertrophy. NaBu significantly attenuated Ang II-induced increase in the mean arterial pressure. Ang II treatment remarkably increased cardiac hypertrophy as indicated by increased ratio of heart weight/body weight and enlarged cardiomyocyte size, extensive fibrosis and inflammation, as well as enhanced expression of hypertrophic markers, whereas hearts from NaBu-treated rats exhibited a significant reduction in these hypertrophic responses. Mechanistically, NaBu inhibited the expression of COX2/PGE2 along with production of ANP and phosphorylated ERK (pERK) stimulated by Ang II in in vivo and in vitro, which was accompanied by the suppression of HDAC5 and HDAC6 activities. Additionally, knocking down the expression of HDAC5 and HDAC6 via gene-editing strategy dramatically blocked Ang II-induced hypertrophic responses through COX2/PGE2 pathway. These results provide solid evidence that NaBu attenuates Ang II-induced cardiac hypertrophy by inhibiting the activation of COX2/PGE2 pathway in a HDAC5/HDAC6-dependent manner.
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