Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence-Immunometabolism-CSCIED科技核心评价数据库-手机版

Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence

Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence

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DOI	10.1097/IN9.0000000000000046
刊名	Immunometabolism IJ
年，卷(期)	2024, 6(3)
作者	Lin, Tonghui; Mohammad, Aftab; Kolonin, Mikhail G.; Eckel-Mahan, Kristin L.,
作者单位	[Lin, Tonghui; Mohammad, Aftab; Kolonin, Mikhail G.; Eckel-Mahan, Kristin L.] Univ Texas Hlth Sci Ctr Houston, Brown Fdn Inst Mol Med, Houston, TX 77030 USA; [Kolonin, Mikhail G.; Eckel-Mahan, Kristin L.] Univ Texas MD Anderson Canc Ctr, UTHlth Grad Sch B
摘要	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.
Abstract	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.
关键词	adipocyte progenitor cells; circadian; aging; senescence; proliferation; adipogenesis
KeyWord	adipocyte progenitor cells; circadian; aging; senescence; proliferation; adipogenesis
基金项目
页码	1-7

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Lin, Tonghui; Mohammad, Aftab; Kolonin, Mikhail G.; Eckel-Mahan, Kristin L.. Mechanisms and metabolic consequences of adipocyte progenitor replicative senescence [J]. Immunometabolism. 2024; 6; (3). 1 - 7.

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