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Spinelli, R.* ; Baboota, R.K.* ; Gogg, S.* ; Beguinot, F.* ; Blüher, M. ; Nerstedt, A.* ; Smith, U.*

Increased cell senescence in human metabolic disorders.

J. Clin. Invest. 133:11 (2023)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
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
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 0021-9738
e-ISSN 1558-8238
Zeitschrift Journal of Clinical Investigation
Quellenangaben Band: 133, Heft: 12, Seiten: , Artikelnummer: 11 Supplement: ,
Verlag American Society of Clinical Investigation
Verlagsort 2015 Manchester Rd, Ann Arbor, Mi 48104 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
POF Topic(s) 30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-506501-001
DOI 10.1172/JCI169922
WOS ID 001023897600005
PubMed ID 37317964
Erfassungsdatum 2024-01-15
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