Inflammaging (inflammation + aging): A driving force for human aging based on an evolutionarily antagonistic pleiotropy theory?
Inflammaging (inflammation + aging): A driving force for human aging based on an evolutionarily antagonistic pleiotropy theory?
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作者：
M. Goto
衰老，特别是人类衰老，可以通过副炎症驱动的炎症的新兴概念来解释，即炎症和衰老的组合。炎症假设生理或病理衰老可以由先天免疫系统产生的促炎细胞因子和物质驱动。动物必须保持稳态，因为他们的年龄，尽管不断攻击从内在和外在的刺激/抗原。这些潜在有害的促炎信号在生命的后期阶段可能会与它们在生命早期阶段的有益作用相对抗，例如作为身体系统形成的发育引擎。炎症的概念是基于在进化过程中编程的拮抗多效性理论。已经提出了包括热量限制、沉默调节蛋白激活剂和p38 MAPK抑制剂的临床试验，以对抗病理性衰老如代谢综合征、糖尿病、类风湿性关节炎和Werner综合征以及生理性衰老。
Aging, and especially human aging, can be explained by the emerging concept of parainflammation-driven inflammaging, i.e. a combination of inflammation and aging. Inflammaging posits that aging either physiologically or pathologically can be driven by the pro-inflammatory cytokines and substances produced by the innate immune system. Animals must maintain homeostasis as they age despite incessant attack from both intrinsic and extrinsic stimuli/antigens. These potentially harmful pro-inflammatory signals at a later stage of life may act antagonistically to the beneficial role they had in an earlier stage of life, like serving as developmental engines for body system formation. The concept of inflammaging is based on an antagonistic pleiotropy theory programmed during evolution. Clinical trials including caloric restriction, sirtuin activators, and p38 MAPK inhibitors against both pathological aging such as metabolic syndrome, diabetes mellitus, rheumatoid arthritis, and Werner syndrome and physiological aging have been proposed.