Author(s)

Mengxin Wen¹, Jing Chai², Beng Wen^3*

¹School of Public Health, Anhui Medical University, Hefei, China.
²School of Clinical Medicine, Wannan Medical College, Wuhu, China.
³Department of Hematology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.

Cellular senescence is a signal transduction process which maintained genomic stability and stopped mammalian cell growth. Furthermore, cellular senescence induces a protective response to a variety of DNA damage. However, this process is also associated with apoptosis, upregulated secretion of inflammatory cytokine, and promoted surrounding tissue damage. When cellular senescence accumulates to a certain extent, it triggers geriatric diseases, such as chronic inflammation, immune senescence-associated tumors and incontrollable infections. Cellular senescence gene SENEX, which was cloned in 2004, has been demonstrated to play a unique gatekeeper function in human endothelial cells when stress-induced pre-mature senescence and apoptosis occurr. The phenomenon that CD4+CD25+ Treg cells accumulated in the aged population has been well studied in recent years. Now Treg accumulation related to immune-pathology has attracted more interest. CD4+CD25+ Treg did not decline and age, but accumulated and suppressed immunoreaction. The enhanced Treg number and function may be associated with stress-induced premature senescence-mediated unique cellular senescence protection mechanisms, and SENEX may play a critical role in this process. In this article, we summarize the cellular senescence and SENEX gene in the accumulation and functional activity of CD4+CD25+ Treg in the elderly.

Cellular Senescence, Gene, SENEX, CD4, CD25, Treg, Elder

Wen, M. , Chai, J. and Wen, B. (2024) Cellular Senescence and SENEX Gene on the Peripheral CD4+CD25+ Treg Cells Enhancement in Elderly. Journal of Biosciences and Medicines, 12, 70-79. doi: 10.4236/jbm.2024.122006.