ArticleCardiovascular toxicology2022
LncRNA MALAT1 Regulates USP22 Expression Through EZH2-Mediated H3K27me3 Modification to Accentuate Sepsis-Induced Myocardial Dysfunction.
Article in Cardiovascular toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Epigenetic mechanisms of Immune remodeling in sepsis: targeting histone modification.Cell death & disease · 2023Pooled it
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- 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
- Neuroepigenetic regulation by long non-coding RNAs in sepsis-associated encephalopathy: cell-type programs and translational biomarkers.Neurogenetics · 2026Review
- Knockdown of SOX4 attenuates sepsis myocardial injury by inhibiting the EZH2/H3K27me3/SOCS3 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- MYSM1-mediated epigenetic modification dysregulation leads to immunosuppression and secondary infections in sepsis.PLoS pathogens · 2026Article
- Progress on Potential Therapeutic Targets for Sepsis-Related Cardiac Dysfunction: From Basic Research to Clinical Translation.ImmunoTargets and therapy · 2026Review
- Knockdown of PATZ1 alleviates chronic heart failure through the USP22/HIF-1α axis.Scientific reports · 2025Article
- The roles of lncMALAT1 in coronary artery disease regulation and therapeutic perspective: A systematic review.iScience · 2025Article
- Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Regulation of histone H3K27 methylation in inflammation and cancer.Molecular biomedicine · 2025Review
- Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.Intensive care medicine experimental · 2025Review
- A new digital droplet PCR method for looking at epigenetics in diffuse large B-cell lymphomas: The role of BMI1, EZH2, and USP22 genes.International journal of laboratory hematology · 2025Article
- The expression of MALAT1, plasma brain natriuretic peptide, and Tei index in sepsis-induced myocardial injury.Journal of cardiothoracic surgery · 2025Article
- Molecular pathology of lymphoma and its treatment strategies: from mechanistic elucidation to precision medicine.Frontiers in immunology · 2025Review
- Is postoperative cognitive dysfunction a disease of microglial inflammatory memory? A state-transition model from metabolic stress to epigenetic lock-in.Frontiers in molecular neuroscience · 2025Review
- miR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury.Toxicology research · 2024Article
- Diagnostic and Predictive Value of LncRNA MCM3AP-AS1 in Sepsis and Its Regulatory Role in Sepsis-Induced Myocardial Dysfunction.Cardiovascular toxicology · 2024Article
- Snhg14/miR-181a-5p axis-mediated "M1" macrophages aggravate LPS-induced myocardial cell injury.Heliyon · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), has been confirmed to recruit enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) to regulate cardiomyocyte apoptosis in diabetic cardiomyopathy. However, whether the similar regulatory axis exists in sepsis-induced myocardial dysfunction (SIMD) has not been clearly established. The current study sought to define the mechanism governing MALAT1-mediated EZH2 in SIMD. MALAT1 was significantly upregulated in lipopolysaccharide-induced cardiomyocytes. Depletion of MALAT1 by caudal vein injection of small interfering RNA targeting MALAT1 alleviated myocardial injury in SIMD rats, restored cardiac function, reduced oxidative stress production and fibrosis, and inhibited inflammatory factors and apoptosis in myocardial tissues. Moreover, MALAT1 bound to EZH2 and promoted EZH2 activity in the nucleus of cardiomyocytes. EZH2 repressed ubiquitin-specific peptidase 22 (USP22) expression through H3K27me3 modification. EZH2 elevation aggravated the cardiac injury in SIMD rats, while USP22 upregulation inhibited the effect of EZH2, which reduced the cardiac injury in SIMD rats. Taken together, MALAT1 decreased USP22 expression by interacting with EZH2, thereby worsening SIMD, highlighting an attractive therapeutic strategy for SIMD.
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