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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
KRT23 as a Potential Target for Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD): Evidence From
Yangmin Hao1,2, Tao Zhang3, Shaliyan Tuerxunmaimaiti1,2
1State Key Laboratory of Pathogenesis, Prevention, and Treatment of High Incidence Diseases in Central Asia, Urumqi, Xinjiang, People's Republic of China.
Background:
Metabolic dysfunction-associated fatty liver disease (MAFLD) is highly prevalent in Xinjiang, with genetic factors influencing its pathogenesis. Keratin 23 (KRT23), a liver-enriched protein linked to metabolic regulation, remains understudied in MAFLD genetics.
Objective:
To investigate associations between KRT23 gene polymorphisms, expression, and MAFLD in Xinjiang.
Methods:
This study enrolled 1,795 MAFLD patients diagnosed via ultrasonography and metabolic criteria. KRT23 polymorphisms (rs72826004, rs2269859) were analyzed. GEO database screening identified MAFLD-related genes. KRT23 expression was assessed in human serum/liver tissues (ELISA, Western blot, qRT‒PCR, IHC) and murine models (high-fat diet-induced MAFLD and db/db mice).
Results:
Enrichment analysis identified 10 key MAFLD-associated genes, including KRT23. The rs72826004 TT genotype increased MAFLD risk (OR: 2.156, P=0.007), while rs2269859 TT conferred protection (OR: 0.306, P=0.002). MAFLD patients exhibited elevated KRT23 protein/mRNA levels in serum and liver versus controls. Murine models confirmed higher KRT23 expression in MAFLD and db/db mice compared to wild-type.
Conclusion:
KRT23 gene polymorphism was associated with the occurrence of MAFLD. The rs72826004 loci TT genotype may be a risk factor for MAFLD, whereas the rs2269859 loci TT genotype may be a protective factor against MAFLD. Higher KRT23 expression (protein and mRNA) is related to MAFLD. KRT23 is a potential target for the treatment of MAFLD.
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