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Review
. 2025 Jan 31;25(1):30.
doi: 10.1007/s10142-025-01544-x.

From fatty liver to fibrosis: the impact of miRNAs on NAFLD and NASH

Affiliations
Review

From fatty liver to fibrosis: the impact of miRNAs on NAFLD and NASH

Reda M Mansour et al. Funct Integr Genomics. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a disease with various levels varying from fatty liver steatosis to acute steatosis which is non-alcoholic steatohepatitis (NASH), which can develop into hepatic failure, as well as in some conditions it can develop into hepatocellular carcinoma (HCC). In the NAFLD and NASH context, aberrant microRNA (miRNA) expression has a thorough contribution to the incidence and development of these liver disorders by influencing key biological actions, involving lipid metabolism, inflammation, and fibrosis. Dysregulated miRNAs can disrupt the balance between lipid accumulation and clearance, exacerbate inflammatory responses, and promote fibrogenesis, thus advancing the severeness of the disorder from simple steatosis to more complex NASH. In the current review, the latest development concerned with the activity of complex regulatory networks of miRNA in the incidence as well as the evolution of NAFLD is to be discussed, also conferring about the miRNAs' role in the onset, pathogenesis as well as diagnosis of NAFLD and NASH discussing miRNAs' role as diagnostic biomarkers and their therapeutic effects on NAFLD/NASH.

Keywords: Diagnosis; Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Therapeutic intervention; miRNAs.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not Applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. Conflict of interest: The author declares they have no conflict of interest. Human and animal ethics: Not applicable.

References

    1. Abu Shelbayeh O, Arroum T, Morris S, Busch KB (2023) PGC-1α is a master regulator of mitochondrial lifecycle and ROS stress response. Antioxidants 12:1075 - PubMed - PMC - DOI
    1. Ahn J, Lee H, Jung CH, Ha T (2012) Lycopene inhibits hepatic steatosis via micro RNA-21‐induced downregulation of fatty acid‐binding protein 7 in mice fed a high‐fat diet. Mol Nutr Food Res 56:1665–1674 - PubMed - DOI
    1. Akuta N, Kawamura Y, Suzuki F, Saitoh S, Arase Y, Fujiyama S, Sezaki H, Hosaka T, Kobayashi M, Suzuki Y (2016) Analysis of association between circulating miR-122 and histopathological features of nonalcoholic fatty liver disease in patients free of hepatocellular carcinoma. BMC Gastroenterol 16:1–9 - DOI
    1. Alessio E, Bonadio RS, Buson L, Chemello F, Cagnin S (2020) A Single Cell but Many Different Transcripts: A Journey into the World of Long Non-Coding RNAs. 21: 302
    1. Alshehri AS, El-Kott AF, El-Kenawy AE, Khalifa HS, AlRamlawy AM (2021) Cadmium chloride induces non-alcoholic fatty liver disease in rats by stimulating miR-34a/SIRT1/FXR/p53 axis. Sci Total Environ 784:147182 - PubMed - DOI

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