ArticleBMC cell biology2018
PIAS1 protects against myocardial ischemia-reperfusion injury by stimulating PPARγ SUMOylation.
Article in BMC cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- ROS-SUMO Crosstalk in Oxidative Stress: Disease Mechanisms and Reproductive Health.Antioxidants (Basel, Switzerland) · 2026Review
- Electroacupuncture posttreatment attenuates the inflammatory injury in rats after MIRI through PPARγ/NF-κb pathway.Frontiers in cardiovascular medicine · 2025Article
- Peptides Are Cardioprotective Drugs of the Future: The Receptor and Signaling Mechanisms of the Cardioprotective Effect of Glucagon-like Peptide-1 Receptor Agonists.International journal of molecular sciences · 2024Review
- Protein inhibitor of activated STAT1 (PIAS1) alleviates cerebral infarction and inflammation after cerebral ischemia in rats.Heliyon · 2024Article
- Review
- SUMOylation does not affect cardiac troponin I stability but alters indirectly the development of force in response to CaThe FEBS journal · 2022Article
- Knockdown of XIST up-regulates 263294miR-340-5p to relieve myocardial ischaemia-reperfusion injury via inhibiting cyclin D1.ESC heart failure · 2022Article
- CBL knockdown protects cardiomyocytes against hypoxia-reoxygenation injury by downregulating GRB2 expression.Experimental and therapeutic medicine · 2022Article
- Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.Analytical cellular pathology (Amsterdam) · 2022Article
- PIAS1 Alleviates Hepatic Ischemia-Reperfusion Injury in Mice through a Mechanism Involving NFATc1 SUMOylation.Disease markers · 2022Article
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- Natural Products Against Renal FibrosisFrontiers in pharmacology · 2022Review
- PIAS1 alleviates diabetic peripheral neuropathy through SUMOlation of PPAR-γ and miR-124-induced downregulation of EZH2/STAT3.Cell death discovery · 2021Article
- SENP1 modulates microglia-mediated neuroinflammation toward intermittent hypoxia-induced cognitive decline through the de-SUMOylation of NEMO.Journal of cellular and molecular medicine · 2021Article
- Up-regulating microRNA-138-5p enhances the protective role of dexmedetomidine on myocardial ischemia-reperfusion injury mice via down-regulating Ltb4r1.Cell cycle (Georgetown, Tex.) · 2021Article
- miR-135b-3p Promotes Cardiomyocyte Ferroptosis by Targeting GPX4 and Aggravates Myocardial Ischemia/Reperfusion Injury.Frontiers in cardiovascular medicine · 2021Article
- SUMO-specific Isopeptidases Tuning Cardiac SUMOylation in Health and Disease.Frontiers in molecular biosciences · 2021Review
- SUMOylation as a Therapeutic Target for Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Review
- The E3 Ligase PIAS1 Regulates p53 Sumoylation to Control Stress-Induced Apoptosis of Lens Epithelial Cells Through the Proapoptotic Regulator Bax.Frontiers in cell and developmental biology · 2021Article
- SUMOylation Connects Cell Stress Responses and Inflammatory Control: Lessons From the Gut as a Model Organ.Frontiers in immunology · 2021Review
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
backgroundMyocardial ischemia-reperfusion injury (IRI) has become one of the most serious complications after reperfusion therapy in patients with acute myocardial infarction. Small ubiquitin-like modification (SUMOylation) is a reversible process, including SUMO E1-, E2-, and E3-mediated SUMOylation and SUMO-specific protease-mediated deSUMOylation, with the latter having been shown to play a vital role in myocardial IRI previously. However, little is known about the function and regulation of SUMO E3 ligases in myocardial IRI.
resultsIn this study, we found dramatically decreased expression of PIAS1 after ischemia/reperfusion (I/R) in mouse myocardium and H9C2 cells. PIAS1 deficiency aggravated apoptosis and inflammation of cardiomyocytes via activating the NF-κB pathway after I/R. Mechanistically, we identified PIAS1 as a specific E3 ligase for PPARγ SUMOylation. Moreover, H9C2 cells treated with hypoxia/reoxygenation (H/R) displayed reduced PPARγ SUMOylation as a result of down-regulated PIAS1, and act an anti-apoptotic and anti-inflammatory function through repressing NF-κB activity. Finally, overexpression of PIAS1 in H9C2 cells could remarkably ameliorate I/R injury.
conclusionsCollectively, our findings demonstrate the crucial role of PIAS1-mediated PPARγ SUMOylation in protecting against myocardial IRI.
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