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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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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Review
Schlagwörter
Adipose-tissue; Endothelial-cells; P53; Hyperinsulinemia; Adipocytes; Mechanisms; Obesity; Depots; Age
ISSN (print) / ISBN
0021-9738
e-ISSN
1558-8238
Zeitschrift
Journal of Clinical Investigation
Quellenangaben
Band: 133,
Heft: 12,
Artikelnummer: 11
Verlag
American Society of Clinical Investigation
Verlagsort
2015 Manchester Rd, Ann Arbor, Mi 48104 Usa
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)