I was writing a review article that includes this topic. I'll attempt to explain recent progress in a non-academic manner here.
When a cell in our body got damaged through a challenge (DNA damaging reagents, radiation, UV, etc) or through botched mitosis, the cell can die. But if the damage is not severe enough to kill the cell, the cell would survive. The survived cell can reprogram itself to express senescent proteins as a part of damage repair attempt. At the same time, with somewhat unclear mechanism, the cell can acquire ability to secrete inflammatory cytokines, interleukins and other proteins.
The acquired phenotype is called Senescence-Associated Secretory Phenotype (SASP).
Senescent cells can be recognized and removed by immune cells. Calling out immune cells to get rid of damaged self (senescent cell) was likely the original purpose for SASP.
Funky part is that the secreted proteins can reach the surrounding cells, and can cause inflammation and damage to these healthy cells. The surrounding cells can acquire SASP that way.
Right. SASP can be contagious and can propagate. Imagine Zombie bites (classic slow one) from senescent cells.
https://upload.wikimedia.org/wikipedia/commons/thumb/5/56/Zombies_NightoftheLivingDead.jpg/220px-Zombies_NightoftheLivingDead.jpg
A paper reported that, in human, fat tissues from 31 years old contain about 3% of senescent cells, while those from 71 years old contain about 10%. As fat tissue is pretty big organ in human, they can influence body's function through SASP (so they argued). Many scientists come to believe that SASP is a significant influencing factor on tissue/organ aging and health span.
Then, perhaps, if you can reduce the effects of SASP, you can stay "younger" for longer? Animal-based experiments support this notion.
There are three approaches to reduce SASP.
1. Prevent senescent cells from occurring (which is probably not a good idea, as senescence-activating mechanisms also play roles in preventing cancer).
2. Kill senescent cells selectively by using specific markers or by taking advantage of unique characters of these cells (this approach is what we are working on).
3. Cut off SASP by intervening SASP process or by tweaking signaling involved in SASP. (With this approach, senescent cells themselves may survive, but SASP is inhibited.)
Recent progress in approach 3 has identified some chemicals that can interfere SASP, including rapamycin, JAK inhibitor, p38 MAPK and MK2 inhibitors, glucocorticoid, and metformin (that diabetes medicine).
The list is expanding. We will know more chemicals that can intervene SASP and about mechanisms that cause SASP, in more organ sites.
Sounds promising? But please be cautious and don't take the chemicals for aging prevention purpose yet. I am talking about latest science, and human application requires a series of testing and clinical trials for obvious reasons.
