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Review
. 2020 Sep 30:11:582368.
doi: 10.3389/fgene.2020.582368. eCollection 2020.

Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning

Sijie Li  1   2 , Changhong Ren  1   2 , Christopher Stone  3 , Ankush Chandra  3 , Jiali Xu  1 , Ning Li  1 , Cong Han  4 , Yuchuan Ding  3 , Xunming Ji  1 , Guo Shao  1   2   5   6
Affiliations
Review

Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning

Sijie Li et al. Front Genet. .

Abstract

Hypoxic/ischemic preconditioning (HPC/IPC) is an innate neuroprotective mechanism in which a number of endogenous molecules are known to be involved. Tuberous sclerosis complex 1 (TSC1), also known as hamartin, is thought to be one such molecule. It is also known that hamartin is involved as a target in the rapamycin (mTOR) signaling pathway, which functions to integrate a variety of environmental triggers in order to exert control over cellular metabolism and homeostasis. Understanding the role of hamartin in ischemic/hypoxic neuroprotection will provide a novel target for the treatment of hypoxic-ischemic disease. Therefore, the proposed molecular mechanisms of this neuroprotective role and its preconditions are reviewed in this paper, with emphases on the mTOR pathway and the relationship between the expression of hamartin and DNA methylation.

Keywords: TSC1; hamartin; hypoxia; ischemia; neuroprotection.

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Figures

FIGURE 1
FIGURE 1
Schematic representation of the hamartin protein and its functional domains. T2BD: TSC2-binding domain; Coil: predicted coiled-coil domain.
FIGURE 2
FIGURE 2
Proposed pathway governing the expression and activity of hamartin under hypoxic/ischemic conditions.
See this image and copyright information in PMC

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