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The way mitochondrial dysfunction likely becomes more manifest in ME/CFS is when symptoms are provoked and de novo energy production is required Its not that the mitochondria are not involved they are but the mitochondrial problems are secondary to the neuroinflammation and oxidative stress thats present

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And in many ways I kind of see that as the first chapter in not just a new mechanism, but mechanistically informed therapeutics

Similarly, excessive ER- receptors in the endothelial cells of the uterine microvasculature induce cyclooxygenase (COX) and prostaglandin-E2 (PGE 2 ) [72]