Invited LecturesCellular Senescence as a Stress ResponseIshikawa, Fuyuki MD, PhDAuthor Information From the Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Kyoto, Japan. Accepted for publication June 6, 2006. Supported by grants-in-aid for cancer research from the Japanese Ministry of Education, Culture, Sports, Science and Technology. Reprints: F. Ishikawa, Laboratory of Cell Cycle Regulation, Department of Gene Mechanisms, Graduate School of Biostudies, Kyoto University, Yoshida-Konoe-cho, Kyoto 606-8501, Japan (e-mail: email@example.com). Cornea: December 2006 - Volume 25 - Issue - p S3-S6 doi: 10.1097/01.ico.0000247206.47897.92 Buy Metrics Abstract Purpose: This review discusses cellular senescence, the state in which normal cells do not respond to growth stimuli, and shows characteristic alterations in their cytologic and biochemical properties and their gene expression profiles. Methods and Results: Cellular senescence is elicited by various stresses. It was recently shown that the stress-induced mitogen-activated protein kinase p38 has a pivotal role in inducing cellular senescence. This finding provided biochemical evidence to support the notion that cellular senescence is a kind of stress response. Conclusion: Stress responses are typically found in cells and organisms surviving unfavorable environmental conditions. It can be argued that cellular senescence is an adaptive process that maintains the cell's viability by reducing the energy consumed for reproduction (ie, cell division) and differentiation-related activities. © 2006 Lippincott Williams & Wilkins, Inc.