The Latest on Cellular Senescence in Type 2 Diabetes

One of the more unexpected recent findings relating to cellular senescence is that it appears to be an important part of the mechanisms that lead to loss of the pancreatic β-cells responsible for insulin secretion in both type 1 diabetes and type 2 diabetes - which are very different conditions, despite the shared name. The authors of the brief open access commentary noted here discuss the present state of this research. Age is one of the major risk factors for the development of type 2 diabetes mellitus (T2D). However, the understanding of how cellular aging contributes to diabetes pathogenesis is incomplete and as a result, current therapies do not target this aspect of the disease. In recent work we showed that insulin resistance induced the expression of aging markers, suggesting that β-cell aging could accelerate the progression toward diabetes. Therefore, reversing the hallmarks of cellular aging presents a potential avenue for novel T2D therapies; in particular, transcriptomic analysis of aged β-cells pointed us toward cellular senescence as a promising target. Senescent cells enter a state of long-term growth inhibition and replicative arrest after exposure to environmental insults, including genomic damage, oncogene activation, and reactive oxygen species. The resulting changes in gene expression impair cell function and proliferation while modifying intercellular signaling through the senescence-associated secretory phenotype (SASP). The potential...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs