ArticleCardiovascular therapeutics2018
TGR5 activation induces cytoprotective changes in the heart and improves myocardial adaptability to physiologic, inotropic, and pressure-induced stress in mice.
Article in Cardiovascular therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Ursodeoxycholic Acid Attenuates Lipopolysaccharide-Induced Myocardial Injury by Inhibiting Oxidative Stress, Inflammation, and Apoptosis: The Interplay of Sirt1/Nrf2 and Akt/NF-κB Signaling Pathways.International journal of molecular sciences · 2026Article
- Classification of intestinal inflammation driven by gut microbiota metabolites: a new paradigm for precision treatment of cardiovascular diseases.Frontiers in microbiology · 2026Review
- Role of Gut Microbiota in Diabetic HFpEF: Mechanisms and Therapeutic Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Microbiome and Heart Failure: A Comprehensive Review of Gut Health and Microbiota-Derived Metabolites in Heart Failure Progression.Medical sciences (Basel, Switzerland) · 2025Review
- The Critical Role of the Bile Acid Receptor TGR5 in Energy Homeostasis: Insights into Physiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Gut-Heart Axis: The Role of Gut Microbiota and Metabolites in Heart Failure.Circulation research · 2025Review
- Yixintai treats chronic heart failure in rats by regulating gut microbiota and bile acid.Frontiers in microbiology · 2025Article
- The bidirectional regulatory mechanism of gut microbiota metabolites on myocardial injury in heart failure from the perspective of the gut-heart axis: a review.Frontiers in microbiology · 2025Review
- The gut microbiota-inflammation-HFpEF axis: deciphering the role of gut microbiota dysregulation in the pathogenesis and management of HFpEF.Frontiers in cellular and infection microbiology · 2025Review
- Cardiac energy metabolic disorder and gut microbiota imbalance: a study on the therapeutic potential of Shenfu Injection in rats with heart failure.Frontiers in microbiology · 2025Article
- Bile acids for diabetic cardiomyopathy.Nature metabolism · 2024Article
- Bile acid metabolism and signaling in health and disease: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Article
- Heart Failure: a Punch from the Gut.Current heart failure reports · 2024Review
- Combined analysis of cecal microbiota and metabolomics reveals the intervention mechanism of Dayuan Yin in acute lung injury.Frontiers in pharmacology · 2024Article
- Mechanistic Review on the Role of Gut Microbiota in the Pathology of Cardiovascular Diseases.Cardiovascular & hematological disorders drug targets · 2024Review
- Protective effect of UDCA against IL-11- induced cardiac fibrosis is mediated by TGR5 signalling.Frontiers in cardiovascular medicine · 2024Article
- From dried bear bile to molecular investigation of differential effects of bile acids inBrain, behavior, & immunity - health · 2023Review
- Recent Advances in Microbiota-Associated Metabolites in Heart Failure.Biomedicines · 2023Review
- The Role of Bile Acids in Cardiovascular Diseases: from Mechanisms to Clinical Implications.Aging and disease · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
introductionAdministration of cholic acid, or its synthetic derivative, 6-alpha-ethyl-23(S)-methylcholic acid (INT-777), activates the membrane GPCR, TGR5, influences whole body metabolism, reduces atherosclerosis, and benefits the cardiovascular physiology in mice. Direct effects of TGR5 agonists, and the role for TGR5, on myocardial cell biology and stress response are unknown.
methodsMice were fed chow supplemented with 0.5% cholic acid (CA) or 0.025% INT-777, a specific TGR5 agonist, or regular chow for 3 weeks. Anthropometric, biochemical, physiologic (electrocardiography and echocardiography), and molecular analysis was performed at baseline. CA and INT-777 fed mice were challenged with acute exercise-induced stress, acute catecholamine-induced stress, and hemodynamic stress induced by transverse aortic constriction (TAC) for a period of 8 weeks. In separate experiments, mice born with constitutive deletion of TGR5 in cardiomyocytes (CM-TGR5
resultsAdministration of CA and INT-777 supplemented diets upregulated TGR5 expression and activated Akt, PKA, and ERK1/2 in the heart. CA and INT-777 fed mice showed improved exercise tolerance, improved sensitivity to catecholamine and attenuation in pathologic remodeling of the heart under hemodynamic stress. In contrast, CM-TGR5
conclusionsBile acids, specifically TGR5 agonists, induce cytoprotective changes in the heart and improve myocardial response to physiologic, inotropic, and hemodynamic stress in mice. TGR5 plays a critical role in myocardial adaptability, and TGR5 activation may represent a potentially attractive treatment option in heart failure.
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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.