Telomere damage activates autophagy to stop cancer

So it turns out that replicative senescence, the process by which short telomeres arrest division, activates autophagy as a mechanism to prevent uncontrolled replicaton and chromosome damage (leading to cancer), whereas DNA damage away from the telomere activates apoptosis (if not repaired).

https://www.scienced...90123131706.htm

https://www.nature.c...1586-019-0885-0

(Abstract only)

Interesting. Besides research, have you found any way to promply apply that knowledge for cancer treatment?

Interesting. Besides research, have you found any way to promply apply that knowledge for cancer treatment?

The main takeaways are that autophagy is good for cancer prevention, and that inhibiting autophagy (with drugs as is sometimes done to kill cancer cells), could be dangerous as it will increase the likelihood of more cancer cells appearing.

A fascinting and relevant paper:

http://emboj.embopre...embj.2018100492

Cardio-myocytes can become senescent and hypertrophic through telomere (length independent) damage. This presumably works via the fragments of telomeric DNA triggering (and eventually overwhelming) autophagy that was described in the paper that started this thread.  This new paper demonstrates this occurs in mice with age. They cleared such cells with senolytics, although with no ready replacements, this is possibly not a good idea (IMO). I wonder if upregulation of autophagy and reducing sterile inflammation might be a better therapy to address these hypertrophic cells.