ArticleRedox biology2019
Resveratrol as a new inhibitor of immunoproteasome prevents PTEN degradation and attenuates cardiac hypertrophy after pressure overload.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- The Heart of the Alzheimer's: A Mindful View of Heart Disease.Frontiers in physiology · 2020Pooled it
- The Potential Protective Effects of Resveratrol Against Cabazitaxel-Induced Oxidative Stress and Cardiotoxicity in Rats.Cardiovascular toxicology · 2026Article
- The role of immunoproteasome in diabetes and diabetes-related complications.Genes & diseases · 2026Review
- Withaferin A Attenuates Angiotensin II-Induced Right Ventricular Dysfunction and Fibrosis.International journal of molecular sciences · 2026Article
- Exosomal Long Noncoding RNA H19 as a Biomarker and Therapeutic Target in Atrial Fibrillation.International journal of biological sciences · 2026Article
- Pharmacological Foundation and Novel Insights of Resveratrol in Cardiovascular System: A Review.Current cardiology reviews · 2026Review
- Targeting oxidative stress-MMP-2 signaling in hypertension-induced cardiovascular remodeling and dysfunction.Frontiers in pharmacology · 2026Review
- Review
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
- Regulatory effects of resveratrol on nitric oxide signaling in cardiovascular diseases.Pharmacological reports : PR · 2025Review
- β-Hydroxybutyrate and Citrate Synthase as Potential Diagnostic Biomarkers in Aging-Related Atrial Fibrillation.Journal of cardiovascular translational research · 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
- The Effects of Resveratrol Supplementation on the Metabolism of Lipids in Metabolic Disorders.Current medicinal chemistry · 2025Review
- Diet induced insulin resistance is due to induction of PTEN expression.Research square · 2024Article
- Searching for Effective Treatments in HFpEF: Implications for Modeling the Disease in Rodents.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Resveratrol inhibits ferroptosis and decelerates heart failure progression via Sirt1/p53 pathway activation.Journal of cellular and molecular medicine · 2023Article
- ATGL deficiency aggravates pressure overload-triggered myocardial hypertrophic remodeling associated with the proteasome-PTEN-mTOR-autophagy pathway.Cell biology and toxicology · 2023Article
- The dichotomous role of immunoproteasome in cancer: Friend or foe?Acta pharmaceutica Sinica. B · 2023Review
- The effects of resveratrol and melatonin on cardiac dysfunction in diabetic elderly female rats.Physiological research · 2023Article
- Ursolic Acid Ameliorates Myocardial Ischaemia/Reperfusion Injury by Improving Mitochondrial Function via Immunoproteasome-PP2A-AMPK Signalling.Nutrients · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sustained cardiac hypertrophy is a major cause of heart failure (HF) and death. Recent studies have demonstrated that resveratrol (RES) exerts a protective role in hypertrophic diseases. However, the molecular mechanisms involved are not fully elucidated. In this study, cardiac hypertrophic remodeling in mice were established by pressure overload induced by transverse aortic constriction (TAC). Cardiac function was evaluated by echocardiography and invasive pressure-volume analysis. Cardiomyocyte size was detected by wheat germ agglutinin staining. The protein and gene expressions of signaling mediators and hypertrophic markers were examined. Our results showed that administration of RES significantly suppressed pressure overload-induced cardiac hypertrophy, fibrosis and apoptosis and improved in vivo heart function in mice. RES also reversed pre-established hypertrophy and restoring contractile dysfunction induced by chronic pressure overload. Moreover, RES treatment blocked TAC-induced increase of immunoproteasome activity and catalytic subunit expression (β1i, β2i and β5i), which inhibited PTEN degradation thereby leading to inactivation of AKT/mTOR and activation of AMPK signals. Further, blocking PTEN by the specific inhibitor VO-Ohpic significantly attenuated RES inhibitory effect on cardiomyocyte hypertrophy in vivo and in vitro. Taken together, our data suggest that RES is a novel inhibitor of immunoproteasome activity, and may represent a promising therapeutic agent for the treatment of hypertrophic diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.