Cutting through the Complexities of mTOR for the Treatment of Stroke
Affiliation: Cellular and Molecular Signaling, Newark, New Jersey 07101, USA.
Keywords: Akt, apoptosis, autophagy, deptor, mammalian target of rapamycin (mTOR), mLST8, mSIN1, mTORC1,
mTORC2, necroptosis, oxidative stress, PI 3-K, PRAS40, Protor-1, p70S6K, raptor, rictor, SGK1, stroke.
On a global basis, at least 15 million individuals suffer some form of a stroke every year. Of these individuals,
approximately 800,000 of these cerebrovascular events occur in the United States (US) alone. The incidence of stroke in
the US has declined from the third leading cause of death to the fourth, a result that can be attributed to multiple factors
that include improved vascular disease management, reduced tobacco use, and more rapid time to treatment in patients
that are clinically appropriate to receive recombinant tissue plasminogen activator. However, treatment strategies for the
majority of stroke patients are extremely limited and represent a critical void for care. A number of new therapeutic
considerations for stroke are under consideration, but it is the mammalian target of rapamycin (mTOR) that is receiving
intense focus as a potential new target for cerebrovascular disease. As part of the phosphoinositide 3-kinase (PI 3-K) and
protein kinase B (Akt) cascade, mTOR is an essential component of mTOR Complex 1 (mTORC1) and mTOR Complex
2 (mTORC2) to govern cell death involving apoptosis, autophagy, and necroptosis, cellular metabolism, and gene
transcription. Vital for the consideration of new therapeutic strategies for stroke is the ability to understand how the
intricate and complex pathways of mTOR signaling sometimes lead to disparate clinical outcomes.
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