ArticleEuropean journal of medical research2024
Regulation of mitochondrial autophagy by lncRNA MALAT1 in sepsis-induced myocardial injury.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Elevated Metastasis-Associated lung adenocarcinoma transcript 1 (MALAT1) expression predicts coronary artery disease severity as a potential biomarker for risk stratification: a cross-sectional study.Annals of medicine · 2026Article
- WTAP-Driven m6A Modification of TIMP1 mRNA Promotes Sepsis-Induced Cardiomyocytes Injury.Biochemical genetics · 2026Article
- Identification of immune cell mitochondrial dysfunction characteristics and clinical predictive biomarkers in sepsis via multi-cohort machine learning and single-cell RNA sequencing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Echoes in the powerhouse: mito-lncRNAs contribution to cardiac function and disease.Acta pharmacologica Sinica · 2026Review
- Methyltransferase METTL1 Upregulates USF2 in a m7G-Dependent Manner to Accelerate Septic Cardiomyopathy by Inactivating PINK1/Parkin-Mediated Mitophagy.Cardiovascular toxicology · 2026Article
- mRedox biology · 2026Review
- Expression characteristics of peripheral blood miR-146a and TLR4 in septic cardiomyopathy: Correlations with myocardial injury markers and cardiac function classification.Pakistan journal of medical sciences · 2026Article
- Correlation analysis of serum PDK4, NLRP3, and PTEN levels in myocardial injury with sepsis.Journal of medical biochemistry · 2026Article
- Neuroepigenetic regulation by long non-coding RNAs in sepsis-associated encephalopathy: cell-type programs and translational biomarkers.Neurogenetics · 2026Review
- Mitochondrial dysfunction and programmed cell death in Alzheimer's disease: A retrospective bioinformatics study.Medicine · 2026Article
- Albumin administration and 28-day mortality in sepsis-induced myocardial injury: a propensity score-matched analysis.Frontiers in pharmacology · 2026Article
- Therapeutical progress in sepsis-induced cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Long non-coding RNA EPB41L4A-AS1 as a biomarker of sepsis alleviates inflammatory response by targeting miR-146a-5p.European journal of medical research · 2025Article
- MEK5-ERK5 pathway mediates mitophagy by regulating Nur77 to promote tumorigenesis of osteosarcoma cells.European journal of medical research · 2025Article
- Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.Intensive care medicine experimental · 2025Review
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6 authors.
Funding
Abstract
backgroundSepsis-induced myocardial injury (SIMI) is a severe complication of sepsis, contributing significantly to mortality. Mitochondrial dysfunction and dysregulated autophagy are implicated in SIMI pathogenesis. Long non-coding RNA MALAT1 has been associated with various diseases, including sepsis, but its role in SIMI remains unclear.
objectiveThis study aimed to investigate the role of lncRNA MALAT1 in SIMI, specifically in the regulation of mitochondrial autophagy.
methodsA sepsis-induced cardiomyopathy model was established in mice, and the cardiac tissues were analyzed. The expression of lncRNA MALAT1 was modulated and its effects on mitochondrial autophagy, myocardial injury, inflammation, and apoptosis were assessed. Furthermore, the interaction between MALAT1 and miR-146a was explored, as well as the involvement of the TLR4/NF-kB/MAPK signaling pathway.
resultsActivation of mitochondrial autophagy by urolithin A (UA) alleviated SIMI, inflammation, and cardiac dysfunction. Downregulation of MALAT1 enhanced mitochondrial autophagy, stabilized the mitochondrial membrane potential, and inhibited mitochondrial reactive oxygen species (ROS) production, leading to improved cell viability and reduced myocardial injury. Furthermore, MALAT1 interacted with miR-146a, and their modulation influenced mitochondrial autophagy, myocardial injury, and inflammation. The TLR4/NF-kB/MAPK signaling pathway was implicated in these processes.
conclusionOur findings suggest that lncRNA MALAT1 plays a crucial role in SIMI by modulating miR-146a-mediated mitochondrial autophagy and the TLR4/NF-kB/MAPK signaling pathway. These results provide new insights into the pathogenesis of SIMI and potential therapeutic targets.
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