Evidence map›Paper›PMID 42749453›Full record

ArticleJournal, genetic engineering & biotechnology2026

miR-34a and miR-223 as diagnostic biomarkers for the severity of non-alcoholic fatty liver disease.

Ammar Kadhim Alzubaidi, Farah Abdulwahab Al-Saadi, Yasir B Fadhil

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Article in Journal, genetic engineering & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Ammar Kadhim AlzubaidiInstitute of Genetic Engineering and Biotechnology for postgraduate studies, University of Baghdad, Baghdad, Iraq. Electronic address: ammar.k@ige.uobaghdad.edu.iq.
Farah Abdulwahab Al-SaadiInstitute of Genetic Engineering and Biotechnology for postgraduate studies, University of Baghdad, Baghdad, Iraq.
Yasir B FadhilBiology Department, College of Education, AL-Iraqia University, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) ranges from simple steatosis to non-alcoholic steatohepatitis (NASH) and fibrosis, yet current non-invasive tools lack accuracy in distinguishing these stages. This study aimed to evaluate the circulating miR-34a and miR-223 as biomarkers for NAFLD staging. In this cross-sectional study, 200 participants were equally divided into healthy individuals and patients with steatosis, NASH and fibrosis groups. Serum miRNA expression was measured by stem-loop RT-qPCR and miR-16 was used for normalization, while clinical parameters were measured to validate miRNAs. ANOVA and Kruskal-Wallis tests were used for group comparisons, while ROC analysis and multivariate regression were used to assess the diagnostic performance. Both miRNAs showed significant changes in mean expression across disease stages (p < 0.001). miR-34a increased from controls (1.42-fold) to NASH (41.28-fold), followed by a relative decline in fibrosis (12.84-fold), while miR-223 remained low in steatosis before rising sharply in NASH (42.17-fold). Both miRNAs correlated strongly with ALT, AST, platelet count, and lipid parameters (|r| > 0.6, p < 0.01). The combined miRNA panel accurately differentiated steatosis from NASH (AUC = 0.978; 96% sensitivity; 94% specificity). Both were independently associated with advanced disease (miR-34a: OR = 1.32, 95% CI: 1.18-1.48; miR-223: OR = 1.28, 95% CI: 1.15-1.42; p < 0.001), and patients in the highest quartiles had a 116-fold higher risk. The addition of both miRNAs to clinical models improved AUC from 0.812 to 0.912 (NRI = 0.267, p < 0.001). The expression patterns of miR-34a and miR-223 offered a practical non-invasive approach for staging of NAFLD.

Indexed as

FibrosismiR-223miR-34aNAFLDNASHRT-qPCRSteatosis

Identifiers

PMID42749453
PMCPMC13485669

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.