Fibrosis is a form of malfunction in tissue maintenance and regeneration, in which cells inappropriately build scar-like collagen structures that disrupt normal tissue function. It is perhaps most significant in age-related diseases of the lung, heart, and kidney, but it is a general feature of old tissues. There are no effective and approved treatments capable of reversing fibrosis to any significant degree, but good evidence has arrived in recent years to suggest that senescent cells, one of the root causes of aging, are also an important contributing cause of the regenerative dysfunction that leads to fibrosis. Senolytic therapies capable of selectively removing senescent cells from an organ with fibrosis should prove helpful.
In that context, it is interesting to look over this recent demonstration of attenuated lung fibrosis via metformin treatment. Metformin is thought to modestly slow aging, being a form of calorie restriction mimetic, but as such treatments go, it is notably poor and unreliable. The animal data is highly varied when it comes to practical outcomes on aging and longevity. The beneficial effect on fibrosis observed here is thought to be mediated via mitochondrial function. Given what is known of metformin in aging, cellular
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