ReviewJournal of molecular endocrinology2026
Pancreatic β-cell aging in physiology and diabetes: emerging roles of m6A mRNA methylation.
Review in Journal of molecular endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
Pancreatic β-cells are essential for glucose homeostasis and are particularly vulnerable to age-related stress. Aging is a fundamental biological process characterized by the progressive functional decline of tissues and organs and defined by several interconnected hallmarks. In type 1 and type 2 diabetes, aging is accelerated - manifesting as DNA damage response, endoplasmic reticulum stress, and mitochondrial dysfunction, collectively driving β-cell dysfunction and senescence. N6-methyladenosine (m6A) is the most prevalent internal messenger RNA (mRNA) modification in eukaryotes. Emerging evidence demonstrates that m6A levels change with age in a tissue-specific manner, contributing to cellular dysfunction and age-related disease. In pancreatic β-cells, m6A hypomethylation compromises identity, survival, and function through mechanisms that include the IGF1 and insulin signaling pathways. Understanding how m6A methylation is regulated in aged β-cells may uncover new therapeutic strategies aimed at preserving β-cell functional mass and promoting healthy aging. This review focuses on pancreatic β-cell aging in physiological and diabetic conditions and examines the emerging role of m6A methylation in aging and diabetes progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.