When animal tissues grow old, the tissues can accumulate senescent cells. Senescent cells can be generated when a cell was damaged but did not die. Senescent cells express some specific proteins that block the cell to start dividing again. That way, senescent cells are not going to proliferate. Unless they are removed (presumably by immune cells or by other causes), they are there among other cells.
My research specialty is Chromosome Instability. Cells with Chromosome Instability end up with getting damaged through mitotic errors, and they can become senescent cells as well.
In the last 10 years or so, biologists came to know that senescent cells are secreting some factors and inflammatory cytokines that can poison, damage, and "age" surrounding tissue. Aging was contagious (!), at least in the cellular level.
A recent paper "MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation", appeared in Nature Cell Biology (another prestigious journal), reported that SASP can be inhibited by a drug Rapamycin (Sirolimus).
Rapamycin is a compound produced by bacteria and is known as immuno-suppressant, thus taken by recipients of organ transplant. Rapamycin is also used for cancer therapy.
An interesting fact is that mice fed with Rapamycin lived 28-38% longer (9-14% in total lifespan).
This new paper gave an explanation; Rapamycin inhibits SASP, and cancels negative effects of senescent cells on surrounding tissue. Since negative effects of aging was at least partially cancelled, the tissues could function better, and the mice could live longer.
I don't fancy taking Rapamycin myself yet. Rapamycin is immunosuppressant, and can increase the risk of serious infection and some cancers. But with refinement, advancement in biology and cellular-level understanding in our body may provide ways to improve quality of life greatly. What if your anti-aging night cream is inhibiting SASP?
[Notion of SASP and age-related disease, from a review by Ovadya and Krizhanovsky, Biogerontology (2014)]
