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Increased cell senescence in human metabolic disorders.
J. Clin. Invest. 133:11 (2023)
Cell senescence (CS) is at the nexus between aging and associated chronic disorders, and aging increases the burden of CS in all major metabolic tissues. However, CS is also increased in adult obesity, type 2 diabetes (T2D), and nonalcoholic fatty liver disease independent of aging. Senescent tissues are characterized by dysfunctional cells and increased inflammation, and both progenitor cells and mature, fully differentiated and nonproliferating cells are afflicted. Recent studies have shown that hyperinsulinemia and associated insulin resistance (IR) promote CS in both human adipose and liver cells. Similarly, increased CS promotes cellular IR, showing their interdependence. Furthermore, the increased adipose CS in T2D is independent of age, BMI, and degree of hyperinsulinemia, suggesting premature aging. These results suggest that senomorphic/senolytic therapy may become important for treating these common metabolic disorders.
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Publication type
Article: Journal article
Document type
Review
Keywords
Adipose-tissue; Endothelial-cells; P53; Hyperinsulinemia; Adipocytes; Mechanisms; Obesity; Depots; Age
ISSN (print) / ISBN
0021-9738
e-ISSN
1558-8238
Quellenangaben
Volume: 133,
Issue: 12,
Article Number: 11
Publisher
American Society of Clinical Investigation
Publishing Place
2015 Manchester Rd, Ann Arbor, Mi 48104 Usa
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)