Abstract
Commentary: Rapalink-1 Increased Infarct Size in Early Cerebral Ischemia-Reperfusion With Increased Blood-Brain Barrier Disruption.
Highlights
We read with great interest the article by Chi et al investigating the effect of inhibiting mammalian target of rapamycin with a third generation mTOR inhibitor, Rapalink-1, in an experimental model of stroke (Chi et al, 2021)
We have shown during global ischemia, resistant cells within the hippocampus (CA3) can up-regulate hamartin leading to mTORC1 inhibition, increasing productive autophagy to promote cell survival
Chi et al used 2 mg/kg of Rapalink-1, which was associated with mTORC1 and mTORC2 inhibition and increased infarct volume (Chi et al, 2021). These findings further highlight the importance of mTORC2 signaling for cell survival during ischemia and suggest that the dose of Rapalink-1 used is not too dissimilar to cytoprotective doses of rapamycin, the increased potency of Rapalink-1 may have resulted in mTORC2 inhibition at a lower dose
Summary
We read with great interest the article by Chi et al investigating the effect of inhibiting mammalian target of rapamycin (mTOR) with a third generation mTOR inhibitor, Rapalink-1, in an experimental model of stroke (Chi et al, 2021). Rapalink-1 increased stroke size which was associated with reduced activity of both mTORC1 and mTORC2. In this commentary we wish to use insights provided by Chi et al to clarify the emerging inconsistencies in the literature surrounding the brain cytoprotective potential of mTOR inhibition in stroke, and the different roles of mTORC1 and mTORC2.
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