mTORC1, Autophagy, and Rapamycin in ME/CFS
This discussion is an extension of the previously described in summary the consequences of chronic mTOR activation in Chronic activation of the mTOR pathway has significant implications for cellular and organismal health : previous article on chronic mTOR activation . At the Community Symposium on the Molecular Basis of ME/CFS , on 9/11/2026, David Kaufman presented a proposed connection between mTORC1 activation, impaired autophagy, mitochondrial dysfunction, inflammation, and ME/CFS , together with the possibility of using rapamycin (sirolimus) to modify this pathway. mTORC1 and autophagy mTORC1 is an important cellular sensor of nutrients, energy availability, growth signals, and stress. When mTORC1 is active, it promotes growth and protein synthesis while suppressing autophagy . Autophagy is the cell's recycling and quality-control system: Damaged proteins/mitochondria → autophagosome → lysosome → degradation → recycling A particularly important component is mitophagy ...
