ArticleJournal of translational medicine2022
Rhein attenuates angiotensin II-induced cardiac remodeling by modulating AMPK-FGF23 signaling.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed, 19 citations in OpenAlex.
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Hydrogels loaded with different substances for treating heart failure: a promising therapy.Frontiers in cardiovascular medicine · 2026Review
- From Gut to Heart: Targeting Trimethylamine N-Oxide as a Novel Strategy in Heart Failure Management.Biomolecules · 2025Review
- Rhein Inhibits Microglia-Mediated Neuroinflammation and Neuronal Damage of Alzheimer's Disease via Regulating the Glutamine-Aspartate-Arginine-NO Metabolic Pathway.International journal of molecular sciences · 2025Article
- Rhein: An Updated Review Concerning Its Biological Activity, Pharmacokinetics, Structure Optimization, and Future Pharmaceutical Applications.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Rhein Alleviates Doxorubicin-Induced Myocardial Injury by Inhibiting the p38 MAPK/HSP90/c-Jun/c-Fos Pathway-Mediated Apoptosis.Cardiovascular toxicology · 2024Article
- 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
- Natural Products from Herbal Medicine Self-Assemble into Advanced Bioactive Materials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Rhein alleviates myocardial ischemic injury by inhibiting mitochondrial division, activating mitochondrial autophagy and suppressing myocardial cell apoptosis through the Drp1/Pink1/Parkin pathway.Molecular biology reports · 2024Article
- The potential of herbal drugs to treat heart failure: The roles of Sirt1/AMPK.Journal of pharmaceutical analysis · 2024Review
- Mitochondrial dysfunction is a key link involved in the pathogenesis of sick sinus syndrome: a review.Frontiers in cardiovascular medicine · 2024Review
- Retinal Microenvironment-Protected Rhein-GFFYE Nanofibers Attenuate Retinal Ischemia-Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Rhein-attenuates LPS-induced acute lung injury via targeting NFATc1/Trem2 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Angiotensin II-Related Activation of Scleral Fibroblasts and Their Role on Retinal Ganglion Cell Death in Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Role of anthraquinones in combating insulin resistance.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidence indicates that myocardial oxidative injury plays a crucial role in the pathophysiology of cardiac hypertrophy (CH) and heart failure (HF). The active component of rhubarb, rhein exerts significant actions on oxidative stress and inflammation. Nonetheless, its role in cardiac remodeling remains unclear.
methodsCH was induced by angiotensin II (Ang II, 1.4 mg/kg/d for 4 weeks) in male C57BL/6 J mice. Then, rhein (50 and 100 mg/kg) was injected intraperitoneally for 28 days. CH, fibrosis, oxidative stress, and cardiac function in the mice were examined. In vitro, neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) pre-treated with rhein (5 and 25 μM) were challenged with Ang II. We performed RNA sequencing to determine the mechanistic role of rhein in the heart.
resultsRhein significantly suppressed Ang II-induced CH, fibrosis, and reactive oxygen species production and improved cardiac systolic dysfunction in vivo. In vitro, rhein significantly attenuated Ang II-induced CM hypertrophy and CF collagen expression. In addition, rhein obviously alleviated the increased production of superoxide induced by Ang II. Mechanistically, rhein inhibited FGF23 expression significantly. Furthermore, FGF23 overexpression abolished the protective effects of rhein on CMs, CFs, and cardiac remodeling. Rhein reduced FGF23 expression, mostly through the activation of AMPK (AMP-activated protein kinase). AMPK activity inhibition suppressed Ang II-induced CM hypertrophy and CF phenotypic transformation.
conclusionRhein inhibited Ang II-induced CH, fibrosis, and oxidative stress during cardiac remodeling through the AMPK-FGF23 axis. These findings suggested that rhein could serve as a potential therapy in cardiac remodeling and HF.
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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 OpenQuestion graph.