In ME/CFS, mitochondrial dysfunction is unlikely a primary driver. Chronic autonomic dysfunction with impaired perfusion and REDOX imbalance ▶️secondary bioenergetic failure. Endoplasmic reticulum stress emerges in parallel, amplifying cellular dysfunction. 
Sympathetic overdrive and regional hypoperfusion alter calcium trafficking and dysfunction at the ER–mitochondria interface ▶️impaired oxidative phosphorylation and increased lactate. Thus, mitochondrial dysfunction may reflect aberrant upstream signaling.
🔷Metformin (activates AMPK)
🔷Pioglitazone (drives PPAR gamma)
🔷GLP-1 agonists (raises cAMP)
🔷Rapamycin (autophagy and mTOR)
🔷TUDCA and NaPB (relieves ER stress)
🔷SS-31 (stabilizes cardiolipin)
The above hypothetically target the signaling layer, not just the mitochondria.
🔷Pioglitazone (drives PPAR gamma)
🔷GLP-1 agonists (raises cAMP)
🔷Rapamycin (autophagy and mTOR)
🔷TUDCA and NaPB (relieves ER stress)
🔷SS-31 (stabilizes cardiolipin)
The above hypothetically target the signaling layer, not just the mitochondria.
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