Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence.

Autor:	Lin T; The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA., Mohammad A; The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA., Kolonin MG; The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA.; Molecular and Translational Biology Program, MD Anderson Cancer Center/UTHealth Graduate School of Biomedical Sciences, Houston, TX, USA.; Department of Integrative Biology and Pharmacology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA., Eckel-Mahan KL; The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA.; Molecular and Translational Biology Program, MD Anderson Cancer Center/UTHealth Graduate School of Biomedical Sciences, Houston, TX, USA.
Jazyk:	angličtina
Zdroj:	Immunometabolism (Cobham, Surrey) [Immunometabolism (Cobham)] 2024 Aug 28; Vol. 6 (3), pp. e00046. Date of Electronic Publication: 2024 Aug 28 (Print Publication: 2024).
DOI:	10.1097/IN9.0000000000000046
Abstrakt:	In recent decades, obesity has become a worldwide epidemic. As a result, the importance of adipose tissue (AT) as a metabolically active storage depot for lipids and a key mediator of body-wide metabolism and energy balance has been increasingly recognized. Emerging from the studies of AT in metabolic disease is a recognition of the importance of the adipocyte progenitor cell (APC) population of AT being the gatekeeper of adipocyte function. APCs have the capability to self-renew and undergo adipogenesis to propagate new adipocytes capable of lipid storage, which is important for maintaining a healthy fat pad, devoid of dysfunctional lipid droplet hypertrophy, inflammation, and fibrosis, which is linked to metabolic diseases, including type 2 diabetes. Like other dividing cells, APCs are at risk for undergoing cell senescence, a state of irreversible cell proliferation arrest that occurs under a variety of stress conditions, including DNA damage and telomere attrition. APC proliferation is controlled by a variety of factors, including paracrine and endocrine factors, quality and timing of energy intake, and the circadian clock system. Therefore, alteration in any of the underlying signaling pathways resulting in excessive proliferation of APCs can lead to premature APC senescence. Better understanding of APCs senescence mechanisms will lead to new interventions extending metabolic health. Competing Interests: The authors declare that they have no conflict of interest. (Copyright © 2024 The Author(s), Published by Wolters Kluwer Health, Inc.)
Databáze:	MEDLINE
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