MiR-92a-3p aggravates myocardial injury and cardiac dysfunction in septic cardiomyopathy by inhibiting Dusp1
4 affiliations
- 1Department of Infectious Diseases, Zhengzhou Central Hospital Affiliated to Zhengzhou University
- 2Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University
- 3Department of Geriatrics, The People’s Hospital of Dazu, Chongqing
- 4Department of Emergency, The Affiliated Changzhou Hospital of Xuzhou Medical University, Changzhou Third People’s Hospital
Abstract
Background This study primarily aims to explore the association between miR-92a-3p and the pathogenesis of septic cardiomyopathy (SCM). Methods To model SCM-induced injury, lipopolysaccharide (LPS) was administered to mice and H9c2 cardiomyocytes. In the in vivo mouse model, left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were quantified via echocardiography. Serum levels of myocardial injury markers (CK-MB/cTnI) and cardiac levels of inflammatory factors (IL-6/IL-1β/TNF-α) were measured using ELISA. For the in vitro cell model, cell proliferative capacity was assessed via CCK-8 assay, and the apoptotic rate was evaluated via flow cytometry. The concentrations of pro-inflammatory factors secreted by H9c2 cells and the levels of intracellular oxidative stress markers (ROS/MDA/SOD) were determined using ELISA and commercial kits. The binding interaction between miR-92a-3p and Dusp1 was confirmed via RNA immunoprecipitation and dual luciferase reporter gene assays. Results Inhibition of miR-92a-3p leads to a significant increase in LVEF and LVFS, while concurrently decreasing the levels of CK-MB, cTnI and inflammatory factors. In H9c2 cells, inhibition of miR-92a-3p results in a significant reduction in apoptosis rate and the expression level of Bax. Concurrently, downregulation of miR-92a-3p suppresses the reduction in cell proliferation. Furthermore, downregulation of miR-92a-3p significantly inhibits the excessive synthesis of pro-inflammatory factors, ROS, and MDA. Dusp1 is a potential target of miR-92a-3p. In LPS-induced cells, downregulation of Dusp1 attenuates the cytoprotective effect mediated by miR-92a-3p inhibitors. Conclusions In SCM, upregulation of miR-92a-3p promotes cardiomyocyte apoptosis, inflammatory response and oxidative stress, and exacerbates cardiac dysfunction by inhibiting Dusp1.
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BibTeX
@article{tao2026mir92a3p,
title = {{MiR-92a-3p aggravates myocardial injury and cardiac dysfunction in septic cardiomyopathy by inhibiting Dusp1}},
author = {Conghui Tao and Yanling Chen and Zheng Zhou and Xu Yu},
journal = {European Journal of Medical Research},
year = {2026},
month = jul,
doi = {10.1186/s40001-026-04881-0},
url = {https://doi.org/10.1186/s40001-026-04881-0},
note = {CC BY},
}
RIS
TY - JOUR
TI - MiR-92a-3p aggravates myocardial injury and cardiac dysfunction in septic cardiomyopathy by inhibiting Dusp1
AU - Conghui Tao
AU - Yanling Chen
AU - Zheng Zhou
AU - Xu Yu
PY - 2026
DA - 2026/07/01
JO - European Journal of Medical Research
DO - 10.1186/s40001-026-04881-0
UR - https://doi.org/10.1186/s40001-026-04881-0
AB - Background This study primarily aims to explore the association between miR-92a-3p and the pathogenesis of septic cardiomyopathy (SCM). Methods To model SCM-induced injury, lipopolysaccharide (LPS) was administered to mice and H9c2 cardiomyocytes. In the in vivo mouse model, left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were quantified via echocardiography. Serum levels of myocardial injury markers (CK-MB/cTnI) and cardiac levels of inflammatory factors (IL-6/IL-1β/TNF-α) were measured using ELISA. For the in vitro cell model, cell proliferative capacity was assessed via CCK-8 assay, and the apoptotic rate was evaluated via flow cytometry. The concentrations of pro-inflammatory factors secreted by H9c2 cells and the levels of intracellular oxidative stress markers (ROS/MDA/SOD) were determined using ELISA and commercial kits. The binding interaction between miR-92a-3p and Dusp1 was confirmed via RNA immunoprecipitation and dual luciferase reporter gene assays. Results Inhibition of miR-92a-3p leads to a significant increase in LVEF and LVFS, while concurrently decreasing the levels of CK-MB, cTnI and inflammatory factors. In H9c2 cells, inhibition of miR-92a-3p results in a significant reduction in apoptosis rate and the expression level of Bax. Concurrently, downregulation of miR-92a-3p suppresses the reduction in cell proliferation. Furthermore, downregulation of miR-92a-3p significantly inhibits the excessive synthesis of pro-inflammatory factors, ROS, and MDA. Dusp1 is a potential target of miR-92a-3p. In LPS-induced cells, downregulation of Dusp1 attenuates the cytoprotective effect mediated by miR-92a-3p inhibitors. Conclusions In SCM, upregulation of miR-92a-3p promotes cardiomyocyte apoptosis, inflammatory response and oxidative stress, and exacerbates cardiac dysfunction by inhibiting Dusp1.
SN - 2047-783X
ER -