Deleting mice senescent cells to slow aging
Kyoto UniversityPeer-Reviewed Publication
Kyoto, Japan -- Aged and frail people often suffer a decline in tissue reserve capacity during aging. This reserve, called resilience, helps the body maintain homeostasis through various defense, compensation, modulation, and repair responses. When resilience is impaired, elderly people tend to experience a gradual waning of their daily activity and an increase in multimorbidity, or dealing with multiple chronic illnesses.
One major cause of resilience decline is an increase in senescent cells that have stopped dividing. The human body has a natural mechanism for eliminating these cells called senolysis, but as we age this 'clearing' mechanism becomes less efficient.
Senescent cells exert harmful effects through the senescence-associated secretory phenotype, or SASP: the release of pro-inflammatory molecules that can adversely affect surrounding cells. This leads to chronic inflammation and age-related diseases, partly explaining why elderly people suffer impaired resilience. Yet how metabolic resilience is involved in survival capacity and SASP has remained unclear.
- Journal
- Signal Transduction and Targeted Therapy
- Funder
- Japan Society for the Promotion of Science, Japan Agency for Medical Research and Development, French National Cancer Institute