Kudravi S A, Reed M J
Department of Medicine, University of Washington, Seattle 98104, USA.
In Vivo. 2000 Jan-Feb;14(1):83-92.
Aging processes can be described as recognizable series of molecular events within vital organ systems whose dysfunction gradually increase with time (reviewed by [1]). This dysfunction manifests itself as abnormal increases and decreases in gene expression and these events occur at a rate that exceeds the relative rate at which they can be corrected. The outcome of this progression is a steady decline in the capacity to successfully maintain an organism's peak physiology, which occurs approximately around the time of sexual maturation. The resulting changes increase the likelihood that an organism will eventually approach a state of increased vulnerability to disease and ultimately leads to death. Within the context of both wound healing and cancer, molecular mechanisms of aging-related changes affect an organism's ability to repair damaged cells and tissues through disregulation of some common molecular pathways. In the case of the former, wound healing is impaired as a result of an inability to adequately express genes which facilitate escape from cell stasis in order to commence and complete the healing process. In the latter case, the failure of a cell's repair mechanism to correct damage to DNA can lead to neoplastic transformation of a normal cell into one with unlimited growth potential. This review compares several of the molecular and cellular events associated with cancer and wound healing during aging.
衰老过程可被描述为重要器官系统内一系列可识别的分子事件，其功能障碍会随时间逐渐增加（见文献[1]综述）。这种功能障碍表现为基因表达的异常增减，且这些事件的发生速度超过了其可被纠正的相对速度。这种进展的结果是成功维持生物体生理巅峰状态的能力稳步下降，大约在性成熟时就会出现这种情况。由此产生的变化增加了生物体最终进入疾病易感性增加状态的可能性，并最终导致死亡。在伤口愈合和癌症的背景下，衰老相关变化的分子机制通过一些常见分子途径的失调，影响生物体修复受损细胞和组织的能力。就前者而言，由于无法充分表达促进细胞从停滞状态逃逸以便启动和完成愈合过程的基因，伤口愈合受到损害。就后者而言，细胞修复机制无法纠正DNA损伤会导致正常细胞发生肿瘤转化，变成具有无限生长潜力的细胞。本综述比较了衰老过程中与癌症和伤口愈合相关的一些分子和细胞事件。
