ArticleMolecular and cellular biochemistry2022
Increased m6A-RNA methylation and FTO suppression is associated with myocardial inflammation and dysfunction during endotoxemia in mice.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
- DNA/RNA Methylation-Driven Coronary Microvascular Dysfunction: Emerging Pathogenic Mechanisms and Therapeutic Opportunities for Heart Failure in Diabetes.Cardiovascular drugs and therapy · 2026Review
- mRedox biology · 2026Review
- FTO-mediated m6A demethylation of TRIM21 regulates macrophage polarization and attenuates myocardial ischemia-reperfusion injury.Immunologic research · 2026Article
- Identification of FTO as a key m6A demethylase linking immune dysregulation to sepsis pathogenesis.Frontiers in immunology · 2026Article
- Elevated FTO alleviates sepsis‑induced acute kidney injury by regulating macrophage inflammatory phenotypes.International journal of molecular medicine · 2026Article
- FTO in cardiovascular diseases: mechanisms, context dependence, and translational opportunities.Frontiers in cell and developmental biology · 2026Review
- m6A RNA methylation in sepsis-induced cardiomyopathy: direct cardiac mechanisms, emerging therapeutic targets, and translational gaps.Frontiers in medicine · 2026Review
- METTL3-mediated mMolecular biology reports · 2025Review
- RNA Modification in Metabolism.MedComm · 2025Review
- A review of gut failure as a cause and consequence of critical illness.Critical care (London, England) · 2025Review
- Curcumin-induced exosomal FTO from bone marrow stem cells alleviates sepsis-associated acute kidney injury by modulating the m6A methylation of OXSR1.The Kaohsiung journal of medical sciences · 2025Article
- Dexmedetomidine plays a protective role in sepsis-associated myocardial injury by repressing PRMT5-mediated ferroptosis.Toxicology research · 2025Article
- m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs.Small science · 2025Review
- LIN28A-dependent lncRNA NEAT1 aggravates sepsis-induced acute respiratory distress syndrome through destabilizing ACE2 mRNA by RNA methylation.Journal of translational medicine · 2025Article
- RNA m6A methylation regulators in sepsis.Molecular and cellular biochemistry · 2024Review
- Review
- Single-cell transcriptomics reveals writers of RNA modification-mediated immune microenvironment and cardiac resident Macro-MYL2 macrophages in heart failure.BMC cardiovascular disorders · 2024Article
- RhoA/ROCK Pathway Is Upregulated in Experimental Autoimmune Myocarditis and Is Inhibited by Simvastatin at the Stage of Myosin Light Chain Phosphorylation.Biomedicines · 2024Article
- The mCardiovascular diagnosis and therapy · 2024Article
- Immunogenetic Aspects of Sarcopenic Obesity.Genes · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Endotoxemia triggers life-threatening immune and cardiovascular response that leads to tissue damage, multi-organ failure, and death. The understanding of underlying molecular mechanisms is still evolving. N6-methyladenosine (m6A)-RNA modification plays key regulatory role in numerous biological processes. However, it remains unclear whether endotoxemia alters RNA methylation in the myocardium. In the current study, we investigated the effect of lipopolysaccharide (LPS)-induced endotoxemia on m6A-RNA methylation and its implications on myocardial inflammation and left ventricular (LV) function. Following LPS administration, mice showed increases in m6A-RNA methylation in the myocardium with a corresponding decrease in the expression of fat mass and obesity-associated protein (FTO, an m6A eraser/demethylase). The changes were associated with a significant increase in expression of myocardial inflammatory cytokine genes, such as IL-6, TNF-α, IL-1β, and reduced LV function. Moreover, rat cardiomyoblasts (H9c2) exposed to LPS showed similar changes (with increase in m6A-RNA methylation and inflammatory cytokine genes, whereas downregulation of FTO). Furthermore, methylated RNA immunoprecipitation assay showed hypermethylation and increase in the expression of IL-6 and TNF-α genes in LPS-treated H9c2 cells as compared to untreated cells. Interestingly, FTO knockdown in cardiomyocytes mimicked the above effects. Taken together, these data suggest that endotoxemia-induced m6A methylation might play a critical role in expression of cardiac proinflammatory cytokines, and modulation of m6A methylation might limit myocardial inflammation and dysfunction during endotoxemia.
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