Nigam Anjana
Department of Surgery, Pt. J. N. M. Medical College, Raipur, CG, India .
Indian J Dermatol. 2011 Nov;56(6):615-21. doi: 10.4103/0019-5154.91816.
Ageing, also called as senescence, is one of the most complex, intrinsic, biological processes of growing older and resulting into reduced functional ability of the organism. Telomerase, environment, low calorie diets, free radicals, etc., are all believed to affect this ageing process. A number of genetic components of ageing have been identified using model organisms. Genes, mainly the sirtuins, regulate the ageing speed by indirection and controlling organism resistance to damages by exogenous and endogenous stresses. In higher organisms, ageing is likely to be regulated, in part, through the insulin/insulin-like growth factor 1 pathway. Besides this, the induction of apoptosis in stem and progenitor cells, increased p53 activity, and autophagy is also thought to trigger premature organismal ageing. Ageing has also been shown to upregulate expression of inflammatory mediators in mouse adipose tissue. The understanding of pathophysiology of ageing over the past few years has posed tremendous challenges for the development of anti-ageing medicine for targeted therapy. Future research areas must include targeted role of systemic inflammatory markers such as C-reactive protein and interleukin 6 and other biochemical and genetic studies including gene signaling pathways, gene microarray analysis, gene modulation, gene therapy, and development of animal/human models for potential therapeutic measures and evaluations.
衰老,也被称为老化,是生物变老过程中最复杂、最内在的生物学过程之一,会导致生物体功能能力下降。端粒酶、环境、低热量饮食、自由基等都被认为会影响这一衰老过程。利用模式生物已经鉴定出许多与衰老相关的基因成分。基因,主要是沉默调节蛋白,通过间接方式调节衰老速度,并控制生物体对外源和内源应激损伤的抵抗力。在高等生物中,衰老可能部分通过胰岛素/胰岛素样生长因子1途径进行调节。除此之外,干细胞和祖细胞中凋亡的诱导、p53活性的增加以及自噬也被认为会引发生物体过早衰老。衰老还被证明会上调小鼠脂肪组织中炎症介质的表达。在过去几年里,对衰老病理生理学的理解给开发用于靶向治疗的抗衰老药物带来了巨大挑战。未来的研究领域必须包括系统性炎症标志物如C反应蛋白和白细胞介素6的靶向作用,以及其他生化和遗传学研究,包括基因信号通路、基因微阵列分析、基因调控、基因治疗,以及开发用于潜在治疗措施和评估的动物/人类模型。