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Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning
Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning
Sijie Li
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Sijie Li
(Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, China)
Changhong Ren
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Changhong Ren
(Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, China)
Christopher Stone
(Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, United States)
Ankush Chandra
(Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, United States)
Jiali Xu
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Ning Li
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Cong Han
(Department of Neurosurgery, The Fifth Medical Centre of PLA General Hospital, Beijing, China)
Yuchuan Ding
(Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, United States)
Xunming Ji
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Guo Shao
(Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China)
Guo Shao
(Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, China)
Guo Shao
(Public Health Department, Biomedicine Research Center, Basic Medical College, Baotou, China)
Guo Shao
(Baotou Medical College of Neuroscience Institute, Baotou Medical College, Baotou, China)
Journal: Frontiers in Genetics
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• Frontiers Media S.A.
• ISSN: 1664-8021
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.