Differences
This shows you the differences between two versions of the page.
| Both sides previous revisionPrevious revision | |
| steatohepatitis [2025/12/18 21:53] – [non-alcoholic steatohepatitis (NASH)] gary1 | steatohepatitis [2026/05/25 15:27] (current) – [non-alcoholic steatohepatitis (NASH)] gary1 |
|---|
| * **role of miR-93 in MASLD** | * **role of miR-93 in MASLD** |
| * "miR-93 was significantly upregulated in the livers of patients with MASLD and diet-induced obese mice. miR-93 KO mice exhibited reduced hepatic steatosis. Specifically, miR-93 deficiency upregulated genes involved in fatty acid oxidation and downregulated genes associated with cholesterol biosynthesis. Sirtuin 1 (SIRT1) was identified as a direct target of miR-93, and miR-93 KO enhanced SIRT1 expression and activated the LKB1-AMPK signaling pathway. **Niacin treatment downregulated miR-93, ameliorating hepatic steatosis** by enhancing SIRT1 activity" (([[https://www.metabolismjournal.com/article/S0026-0495(25)00135-0/abstract|2025: Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1]])) | * "miR-93 was significantly upregulated in the livers of patients with MASLD and diet-induced obese mice. miR-93 KO mice exhibited reduced hepatic steatosis. Specifically, miR-93 deficiency upregulated genes involved in fatty acid oxidation and downregulated genes associated with cholesterol biosynthesis. Sirtuin 1 (SIRT1) was identified as a direct target of miR-93, and miR-93 KO enhanced SIRT1 expression and activated the LKB1-AMPK signaling pathway. **Niacin treatment downregulated miR-93, ameliorating hepatic steatosis** by enhancing SIRT1 activity" (([[https://www.metabolismjournal.com/article/S0026-0495(25)00135-0/abstract|2025: Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1]])) |
| | * **role of epigentic modifications in NAFLD** |
| | * NUPR1, a stress-induced transcriptional regulator, undergoes m1A modification. YTHDF1 directly binds to m1A-modified NUPR1 mRNA, enhancing its stability, thereby leading to elevated NUPR1 protein levels. Functionally, upregulated NUPR1 acts as a core driver of NAFLD pathogenesis by activating lipogenic and suppressing fatty acid β-oxidation genes, thereby exacerbating hepatic lipid accumulation.(([[https://www.xiahepublishing.com/2310-8819/JCTH-2025-00570|2026: m1A Epitranscriptomic Control of NUPR1 by YTHDF1 Exacerbates Metabolic Dysregulation in Nonalcoholic Fatty Liver Disease]])) |
| |
| =====acute fatty liver of pregnancy (AFLP)===== | =====acute fatty liver of pregnancy (AFLP)===== |
