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首页> 美国卫生研究院文献>Aging (Albany NY) >Embrace the fat when getting old
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Embrace the fat when getting old

机译：变胖时要胖

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Aging is a complex and dynamic disease characterized by a gradual loss of physiological homeostasis, from the cellular to the organismic level, with ultimately fatal consequences. A more systemic understanding of the cell types and pathways at play is required for rational, targeted interventions into this progressing process [ ]. Aging is a normal part of human life-span on the one hand, but associated with many disease risks on the other, indeed, the deterioration frequently exhibited during aging is considered a major risk factor for many human pathologies including type II diabetes mellitus and obesity. Immuno-metabolic derailments accompany the aging process and the development of obesity. Both phenomena therefore share many biological similarities including inflammatory insults and multi-layered cellular and subcellular aberrations [ ]. Examples include altered intercellular communication, mitochondrial dysfunction and deregulated nutrient sensing; all hallmarks of aging that are also characteristic in the context of obesity. Among the other hallmarks of aging are stem cell exhaustion, loss of proteostasis, and cellular senescence [ ]. The clearance of accumulating damaged cells or senescent cells through phagocytosis is a common strategy to counteract these harmful effects, including in the context of the aging process. As such, the immune system has been recently implicated as a central mediator of organ-level homeostasis and can thus help to preserve tissue integrity in anti-aging interventions. However, a fine balance is required to avoid uncontrolled over-activation of such beneficial immune responses, which may predispose to auto-immune consequences. The precise molecular-level characteristics of immune-metabolic interactions, including the involvement of subsets of phagocytes, and ways to specifically recruit and activate them to counteract aging-related metabolic risks and sustain homeostasis, still remain to be identified.
机译：衰老是一种复杂而动态的疾病，其特征是生理稳态从细胞水平到机体水平逐渐丧失，最终导致致命的后果。对于这种进展过程的合理，有针对性的干预，需要对系统中细胞类型和途径的更系统的理解。一方面，衰老是人类寿命的正常组成部分，但另一方面却与许多疾病风险相关，实际上，衰老期间经常出现的恶化被认为是许多人类疾病（包括II型糖尿病和肥胖症）的主要危险因素。免疫代谢脱轨伴随着衰老过程和肥胖症的发展。因此，这两种现象都有许多生物学上的相似之处，包括炎症性损伤以及多层细胞和亚细胞畸变[]。例子包括细胞间通讯改变，线粒体功能障碍和营养感应失调。肥胖背景下的所有衰老特征。衰老的其他标志是干细胞衰竭，蛋白稳态丧失和细胞衰老[]。通过吞噬作用清除积累的受损细胞或衰老细胞是抵消这些有害作用的一种常见策略，包括在衰老过程中。因此，免疫系统最近被认为是器官水平体内平衡的主要调节者，因此可以在抗衰老干预措施中帮助保持组织完整性。但是，需要很好的平衡，以避免这种有益的免疫反应不受控制的过度激活，而过度激活可能会导致自身免疫后果。免疫代谢相互作用的精确分子水平特征，包括吞噬细胞亚群的参与，以及特异性招募和激活它们以抵抗与衰老相关的代谢风险和维持体内稳态的方法，仍有待确定。

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