# MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction

## TL;DR

MiR-143-5p is a potential diagnostic biomarker for sepsis and heart dysfunction, and its overexpression can reduce inflammation and heart damage.

## Contribution

MiR-143-5p is newly identified as a diagnostic biomarker and therapeutic target for sepsis and sepsis-induced cardiac dysfunction.

## Key findings

- MiR-143-5p downregulation is a strong diagnostic indicator for sepsis and sepsis-related cardiac dysfunction.
- Overexpression of miR-143-5p reduces inflammation in macrophages and protects cardiomyocytes from injury.
- MiR-143-5p is linked to p53 and MAPK signaling pathways in sepsis.

## Abstract

Background & Objective. MicroRNAs (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.

The online version contains supplementary material available at 10.1186/s41065-025-00623-0.