Surprising results here, showing that treatment of mice with canagliflozin leads to reduction of senescent cell burden through AMPK activation.
It will be important to learn whether the AICAR/AMPK pathway is activated as a consequence of glucose moderation or as something independent. The authors attempt to show that this effect is glucose independent by using an insulin-treated control group, but this is a bad control in my opinion. It is also too bad that they didn’t include female mice, as that could offer clues as to the relevance of these results for lifespan extension.
SGLT2 inhibition eliminates senescent cells and alleviates pathological aging
Interesting. Why does AMPK activation reduce the number of senescent cells? I thought energy deficiency (turn up AMPK) would turn down the immune system. Perhaps it is the upregulation of autophagy that stops cells from becoming senescent which is causing the pool of senescent cells to shrink (with the help of the immune system).
Total senescent burden = existing senescent cells plus new senescent cells minus senescent cells removed by the immune system.
I think you want to add a multiplier to account for the degree of senescence and make room for senomorphic results from drugs like Rapamycin ((senescent cell + new senecent cells) x SASP Coefficient) - immune removal = senecent burden