Work

Diagnostic and prognostic value of serum miR-125a-5p in patients with chronic heart failure

Year: 2026
Type: article
Study design: Observational Study
Abstract: Objectives This work aimed to examine the aberrant expression of miR-125a-5p in chronic heart failure (CHF) patients and assess its clinical significance. Methods Participants included healthy controls and CHF patients. miR-125a-5p levels were analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Multivariate Cox regression analysis identified the risk of CHF development. Receiver Operating Curve (ROC) analysis was conducted to evaluate the diagnostic accuracy of serum miR-125a-5p for CHF. Kaplan-Meier analysis was generated to assess the survival outcomes. A myocardial injury cell model was created by treating cardiomyocytes with doxorubicin (DOX). Cell proliferation was assessed using Cell Counting Kit-8, while apoptosis rates were quantified by flow cytometry. The concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP) was measured using Enzyme-Linked Immunosorbent Assay (ELISA). Results Serum miR-125a-5p levels were significantly reduced in CHF patients. ROC curve analysis revealed an area under the curve (AUC) of 0.9446 for miR-125a-5p in distinguishing CHF from controls. Furthermore, low serum miR-125a-5p expression was significantly associated with poor patient prognosis and emerged as an independent risk factor for adverse outcomes in CHF patients. In vitro experiments demonstrated that DOX treatment significantly suppressed miR-125a-5p expression in cardiomyocytes, leading to inhibited cell proliferation and increased apoptosis. Conversely, overexpression of miR-125a-5p effectively reversed these DOX-induced cellular injury effects and suppressed the upregulation of NT-proBNP expression. Conclusions Serum miR-125a-5p expression is downregulated in patients with CHF and may serve as a novel diagnostic and prognostic biomarker. Its mechanism may involve exerting cardioprotective effects during CHF progression by regulating cardiomyocyte proliferation, apoptosis, and stress responses.
Language: English
Subfield: Cancer Research
Open Access status: gold
Estimated APC paid: $848
OpenAlex ID: W7162194495
FWCI:
Cites: 29
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