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©The Author(s) 2025.
World J Diabetes. Sep 15, 2025; 16(9): 109768
Published online Sep 15, 2025. doi: 10.4239/wjd.v16.i9.109768
Published online Sep 15, 2025. doi: 10.4239/wjd.v16.i9.109768
Figure 1 Schematic of Ras homolog enriched in brain 1 activating mechanistic target of rapamycin complex 1/AMP-activated protein kinase to regulate hepatocyte nuclear factor 4 alpha-dependent β cell proliferation, insulin transcription, identity, and metabolic homeostasis, driving functional β cell expansion.
Rheb1: Ras homolog enriched in brain 1; mTORC1: Mechanistic target of rapamycin complex 1; AMPK: AMP-activated protein kinase; HNF4α: Hepatocyte nuclear factor 4 alpha.
Figure 2 A schematic diagram showing Ras homolog enriched in brain 1-high-expression-mediated β-cell proliferation/function enhancement via dual pathway activation and hepatocyte nuclear factor 4 alpha upregulation, with translational research pipeline.
Rheb1: Ras homolog enriched in brain 1; mTORC1: Mechanistic target of rapamycin complex 1; AMPK: AMP-activated protein kinase; HNF4α: Hepatocyte nuclear factor 4 alpha.
- Citation: Peng Y, Zhang DD, Gan L, Zhang JQ. Targeting Ras homolog enriched in brain 1 to restore β-cell mass and function: A potential therapeutic strategy for diabetes. World J Diabetes 2025; 16(9): 109768
- URL: https://www.wjgnet.com/1948-9358/full/v16/i9/109768.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i9.109768