Hunt Nicholas J, Kang Sun Woo Sophie, Lockwood Glen P, Le Couteur David G, Cogger Victoria C
ANZAC Research Institute, Aging and Alzheimer's Institute, Centre for Education and Research on Ageing, Concord Repatriation General Hospital, Concord, NSW, Australia.
The University of Sydney, Concord Clinical School, Sydney Medical School, Sydney, NSW, Australia.
Comput Struct Biotechnol J. 2019 Aug 7;17:1151-1161. doi: 10.1016/j.csbj.2019.07.021. eCollection 2019.
While the liver demonstrates remarkable resilience during aging, there is growing evidence that it undergoes all the cellular hallmarks of aging, which increases the risk of liver and systemic disease. The aging process in the liver is driven by alterations of the genome and epigenome that contribute to dysregulation of mitochondrial function and nutrient sensing pathways, leading to cellular senescence and low-grade inflammation. These changes promote multiple phenotypic changes in all liver cells (hepatocytes, liver sinusoidal endothelial, hepatic stellate and Küpffer cells) and impairment of hepatic function. In particular, age-related changes in the liver sinusoidal endothelial cells are a significant but under-recognized risk factor for the development of age-related cardiometabolic disease.
虽然肝脏在衰老过程中表现出显著的恢复力,但越来越多的证据表明,它经历了衰老的所有细胞特征,这增加了肝脏疾病和全身性疾病的风险。肝脏的衰老过程是由基因组和表观基因组的改变驱动的,这些改变导致线粒体功能和营养感知途径失调,进而导致细胞衰老和低度炎症。这些变化促使所有肝细胞(肝细胞、肝窦内皮细胞、肝星状细胞和库普弗细胞)发生多种表型变化,并损害肝功能。特别是,肝窦内皮细胞的年龄相关变化是与年龄相关的心脏代谢疾病发生的一个重要但未得到充分认识的危险因素。