Eric Topol posted recently about mitochondrial dysfunction caused by COVID.
Facts, data, and analytics about biomedical matters.
erictopol.substack.com
>>>Even when the virus was cleared and lung mitochondrial function had recovered, mitochondrial function in the heart, kidney, liver, and lymph nodes remained impaired, potentially leading to severe COVID-19 pathology.<<<
Topol states:
>>>Notably, the virus’s suppression of mitochondrial genes inhibited or inactivated the entire OXPHOS complex, forces an alternative pathway to energy production—
essentially hijacking the cells to make more virus.<<<
Topol mentions two drugs that might be candidates to treat this:
>>>Which brings us to potential therapies that would restore intact mitochondrial function, especially those that can be repurposed. There’s a long list of candidates, but the authors specifically mention the mTOR inhibitor rapamycin, which ha
s been studied for improving mitochondrial function as seen below. Another drug that has already been shown to help
prevent Long Covid, metformin, working in this same pathway, without the immune suppression of rapamycin, and very low cost, would also deserve attention for clinical trials.<<<