Programmed cell death and apoptosis in aging and life span regulation.
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.
Shen
Jie
J
Molecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA. jies@usc.edu
Tower
John
J
D000375:Aging / Q000235:genetics / Q000502:physiology*; D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D016923:Cell Death / Q000235:genetics / Q000502:physiology*; D016922:Cellular Senescence / Q000235:genetics / Q000502:physiology; D006801:Humans; D008136:Longevity / Q000235:genetics / Q000502:physiology*; D009369:Neoplasms / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D016159:Tumor Suppressor Protein p53
D016159:Tumor Suppressor Protein p53