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衰老与寿命调控中的程序性细胞死亡和细胞凋亡

Programmed cell death and apoptosis in aging and life span regulation.

作者信息

Shen Jie, Tower John

机构信息

Molecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA.

出版信息

Discov Med. 2009 Dec;8(43):223-6.

Abstract

Increasing evidence suggests an important role for programmed cell death (PCD) pathways in aging phenotypes across species. PCD is critical to the homeostasis of tissues maintained by cell division, for example, the blood and the lining of the gut. During aging, accumulated cellular damage and non-optimal systemic signaling can cause too little cell death (hyperproliferation and cancer), or too much cell death (tissue atrophy and ectopic cell death), thereby limiting tissue function and life span. For these reasons PCD pathways are promising targets for interventions in aging and aging-related diseases: reactivation of PCD may be beneficial in clearing cancerous and senescent cells, whereas inhibiting PCD may help prevent muscle atrophy and nervous system degeneration.

摘要

越来越多的证据表明,程序性细胞死亡(PCD)途径在跨物种衰老表型中起着重要作用。PCD对于由细胞分裂维持的组织稳态至关重要,例如血液和肠道内膜。在衰老过程中,累积的细胞损伤和非最佳的全身信号传导可导致细胞死亡过少(细胞过度增殖和癌症)或细胞死亡过多(组织萎缩和异位细胞死亡),从而限制组织功能和寿命。基于这些原因,PCD途径是衰老及衰老相关疾病干预的有前景的靶点:重新激活PCD可能有利于清除癌细胞和衰老细胞,而抑制PCD可能有助于预防肌肉萎缩和神经系统退化。

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