| Literature DB >> 23454762 |
Abstract
Preservation and regeneration of β cell endocrine function is a long-sought goal in diabetes research. Defective insulin secretion from β cells underlies both type 1 and type 2 diabetes, thus fueling considerable interest in molecules capable of rebuilding β cell secretion capacity. Though early work in rodents suggested that regeneration might be possible, recent studies have revealed that aging powerfully restricts cell cycle entry of β cells, which may limit regeneration capacity. Consequently, aging has emerged as an enigmatic challenge that might limit β cell regeneration therapies. This Review summarizes recent data regarding the role of aging in β cell regeneration and proposes models explaining these phenomena.Entities:
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Year: 2013 PMID: 23454762 PMCID: PMC3582123 DOI: 10.1172/JCI64095
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808