ArticleBioengineered2022
Role of sevoflurane in myocardial ischemia-reperfusion injury via the ubiquitin-specific protease 22/lysine-specific demethylase 3A axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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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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.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Crosstalk between ubiquitination and other post-translational modifications in cardiovascular diseases.iScience · 2026Review
- The potential of TRPC channel-mediated autophagy in myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Review
- Deubiquitinase USP7 Regulates Neutrophil Extracellular Trap Formation and Inflammation in Lipopolysaccharide-Treated Mice Through ICAM-1 Expression.The Kaohsiung journal of medical sciences · 2026Article
- Roles of ubiquitin‑specific peptidase 22 in cellular fate: From embryonic survival to tissue repair, inflammation and metabolism (Review).International journal of molecular medicine · 2026Review
- Chaperone-Mediated Autophagic Degradation of USP9X in Macrophages Exacerbates Postmyocardial Infarction Inflammation and Cardiac Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Non-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A.Oncogene · 2026Article
- Knockdown of PATZ1 alleviates chronic heart failure through the USP22/HIF-1α axis.Scientific reports · 2025Article
- Non-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A.Oncogene · 2025Article
- Ubiquitin-specific protease: an emerging key player in cardiomyopathy.Cell communication and signaling : CCS · 2025Review
- The multifaceted anticancer potential of luteolin: involvement of NF-κB, AMPK/mTOR, PI3K/Akt, MAPK, and Wnt/β-catenin pathways.Inflammopharmacology · 2025Review
- Sevoflurane pretreatment alleviates hypoxia-reoxygenation-induced myocardial cell injury by upregulating miR-21-5p.Frontiers in cardiovascular medicine · 2025Article
- Sevoflurane Alleviates Cardiomyocyte Ferroptosis via Ubiquitin-Specific Protease 7/Phosphatase and Tensin Homolog Modulation.Drug design, development and therapy · 2025Article
- USP38 exacerbates pressure overload-induced left ventricular electrical remodeling.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- Exploring anesthetic-induced gene expression changes and immune cell dynamics in atrial tissue post-coronary artery bypass graft surgery.Open medicine (Warsaw, Poland) · 2024Article
- USP22 knockdown protects against cerebral ischemia/reperfusion injury via destabilizing PTEN protein and activating the mTOR/TFEB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Cardioprotection of mAb2G4/ODN/lip on Myocardial Ischemia-Reperfusion Injury via Inhibiting the NF-Cardiovascular therapeutics · 2023Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia-reperfusion injury (MIRI) represents a coronary artery disease, accompanied by high morbidity and mortality. Sevoflurane post-conditioning (SPC) is importantly reported in myocardial disease. Accordingly, the current study sought to evaluate the role of Sevo in MI/RI. Firstly, MI/RI models were established and subjected to SPC. Subsequently, pathological injury in the myocardium, myocardial infarction areas, H9c2 cell viability, apoptosis, and levels of creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), and lactate dehydrogenase (LDH) were all measured. Ubiquitin-specific peptidase (22USP22), lysine-specific demethylase 3A (KDM3A), and Yes1 associated transcriptional regulator (YAP1) were down-regulated in H9c2 cells using cell transfection to verify their roles. The interaction between USP22 and KDM3A and between KDM3A and YAP1 was further validated. USP 22, KDM3A, and YAP1 were found to be down-regulated in MI/RI and SPC protected MI/RI rats, as evidenced by up-regulated expressions of USP22, KDM3A, and YAP1, reduced pathological injury in the myocardium, myocardial infarction areas, apoptosis, and levels of CK-MB, cTnI, and LDH, and enhanced H9c2 cell viability; while the protective effects of Sevo were counteracted by silencing of USP22, KDM3A, and SPC upregulated USP22, which stabilized KDM3A protein levels via deubiquitination, and KDM3A inhibited histone 3 lysine 9 di-methylation (H3K9me2) levels in the YAP1 promoter to encourage YAP1 transcription, to reduce MI/RI.
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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.