ArticleHereditas2025
MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
objectiveMicroRNAs (miRNAs) offer advantages in stability and therapeutic specificity. This study investigated the diagnostic and therapeutic potential of miR-143-5p in sepsis (SP) and SP-associated cardiac dysfunction (CD). Methods. Quantitative Real-Time polymerase chain reaction (qRT-PCR) quantified serum and cellular miR-143-5p levels. Receiver operator characteristic (ROC) curve evaluated miR-143-5p's diagnostic efficacy. Pearson correlation analysis assessed the association between miR-143-5p and SP. Univariate logistic regression identified CD risk factors, with multivariate logistic analysis including significant variables from univariate analysis. Lipopolysaccharide (LPS)-induced macrophage (THP-1) and cardiomyocyte (AC16) models elucidated miR-143-5p mechanisms in SP, with bioinformatics predicting the potential pathways. Results. MiR-143-5p downregulation demonstrated diagnostic value for SP (AUC: 0.897) and SP-CD (AUC: 0.812). MiR-143-5p expression correlated (P < 0.0001) with white blood cell count (WBC, r = -0.680), C-reactive protein (CRP, r = -0.563), procalcitonin (PCT, r = - 0.693), left ventricular ejection fraction (LVEF, r = 0.640), cardiac troponin I (cTnI, r = -0.599), Acute Physiology And Chronic Health Evaluation II (APACHE II, r = -0.695), and Sequential Organ Failure Assessment (SOFA, P < 0.05) scores. MiR-143-5p served as a risk factor for CD in SP (OR: 0.100). MiR-143-5p overexpression reduced M1 polarization and pro-inflammatory cytokines in LPS-treated THP-1. In AC16 cardiomyocytes, it enhanced viability, suppressed apoptosis, and attenuated inflammation. Bioinformatics analysis indicated miR-143-5p was involved in p53 and MAPK signal pathways regulation. Conclusions. MiR-143-5p downregulation showed diagnostic potential for SP and SP with CD, correlating with disease severity and CD risk. Mechanistically, miR-143-5p overexpression mitigated macrophage and cardiomyocyte injury.
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