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Diagnostic value of miR-126-5p in sepsis-induced acute kidney injury and its molecular mechanism via CASP3.

Created on 05 Jul 2026

Authors

Xiaowei Yuan, Wanyi Tan, Yuan Zhang, Lin He

Published in

Shock (Augusta, Ga.). Jul 03, 2026. Epub Jul 03, 2026.

Abstract

As a common and devastating complication of sepsis, sepsis-induced acute kidney injury (SAKI) confers a significant risk of mortality.
This work focused on the utility of miR-126-5p as a biomarker for SAKI.
A total of 95 patients with SAKI and 70 patients with sepsis alone were enrolled. Serum levels of miR-126-5p and Caspase-3 (CASP3) were measured using RT-qPCR. The regulatory interaction between miR-126-5p and CASP3 was validated using a dual-luciferase reporter assay. Cell proliferation, apoptosis, inflammatory cytokine levels, and oxidative stress markers were evaluated using the CCK-8 assay, flow cytometry, ELISA, and corresponding commercial kits, respectively.
Serum miR-126-5p levels were downregulated in SAKI patients and showed significant negative correlations with kidney injury markers, including serum creatinine (Scr), cystatin C (Cys-C), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1). Overexpression of miR-126-5p in lipopolysaccharide (LPS)-stimulated HK-2 cells was shown in vitro to facilitate cell proliferation, restrain apoptosis, and suppress the production of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Concurrently, it reduced oxidative stress markers, reactive oxygen species (ROS), and malondialdehyde (MDA), and enhanced superoxide dismutase (SOD) activity. Mechanistically, CASP3 was identified as a direct downstream target of miR-126-5p, and its expression was negatively regulated by miR-126-5p. Furthermore, overexpression of CASP3 significantly reversed the protective effects of miR-126-5p in vitro.
MiR-126-5p showed diagnostic value for SAKI and exerted a protective effect in vitro through targeted regulation of CASP3 expression.

PMID:
42401483
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.

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