Targeting Ras homolog enriched in brain 1 to restore β-cell mass and function: A potential therapeutic strategy for diabetes
Abstract
This editorial highlighted the central role of pancreatic β-cell dysfunction in the pathogenesis of diabetes mellitus and discussed the emerging significance of Ras homolog enriched in brain 1 (Rheb1) as a key regulator of β-cell mass and insulin-secretory capacity. While molecular mechanisms governing β-cell homeostasis remain incompletely defined, Yang et al have recently demonstrated that Rheb1 could promote β-cell proliferation through dual activation of mechanistic target of rapamycin complex 1 and AMP-activated protein kinase signaling pathways, rather than relying solely on mechanistic target of rapamycin complex 1. Notably, Rheb1 expression is higher in pancreatic islets from younger individuals and upregulates hepatocyte nuclear factor 4 alpha, which is recognized as a transcription factor essential for β-cell identity and insulin production. These insights position Rheb1 as a pivotal regulator of β-cell growth and metabolic function, with potential therapeutic implications for diabetes. Targeting Rheb1 may shift treatment paradigms from conventional glucose-lowering strategies toward β-cell restoration, providing a novel approach to preserve or enhance functional β-cell mass in diabetic patients. Further investigation into Rheb1's upstream regulators and downstream effectors may provide innovative therapeutic directions.
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