title: Preconditioning in neuroprotection: From hypoxia to ischemia.
abstract: Sublethal hypoxic or ischemic events can improve the tolerance of tissues, organs, and even organisms from subsequent lethal injury caused by hypoxia or ischemia. This phenomenon has been termed hypoxic or ischemic preconditioning (HPC or IPC) and is well established in the heart and the brain. This review aims to discuss HPC and IPC with respect to their historical development and advancements in our understanding of the neurochemical basis for their neuroprotective role. Through decades of collaborative research and studies of HPC and IPC in other organ systems, our understanding of HPC and IPC-induced neuroprotection has expanded to include: early- (phosphorylation targets, transporter regulation, interfering RNA) and late- (regulation of genes like EPO, VEGF, and iNOS) phase changes, regulators of programmed cell death, members of metabolic pathways, receptor modulators, and many other novel targets. The rapid acceleration in our understanding of HPC and IPC will help facilitate transition into the clinical setting.
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China; National Clinical Research Center for Geriatric Disorders, Beijing, China.
authors.forename: Sijie
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: Adam
authors.initials: A
authors.lastname: Hafeez
authors.affiliation: Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: Fatima
authors.initials: F
authors.lastname: Noorulla
authors.affiliation: Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA; Department of Neurology, Luhe Hospital, Capital Medical University, Beijing, China.
authors.forename: Xiaokun
authors.initials: X
authors.lastname: Geng
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China.
authors.forename: Guo
authors.initials: G
authors.lastname: Shao
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China.
authors.forename: Changhong
authors.initials: C
authors.lastname: Ren
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China.
authors.forename: Guowei
authors.initials: G
authors.lastname: Lu
authors.affiliation: Department of Neurosurgery, Stanford University, CA, USA.
authors.forename: Heng
authors.initials: H
authors.lastname: Zhao
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China; Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: Yuchuan
authors.initials: Y
authors.lastname: Ding
authors.affiliation: Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuan Wu Hospital, Capital Medical University, Beijing, China; National Clinical Research Center for Geriatric Disorders, Beijing, China. Electronic address: jixm@ccmu.edu.cn.
authors.forename: Xunming
authors.initials: X
authors.lastname: Ji
mesh_terms: D000818:Animals; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology / Q000628:therapy; D007511:Ischemia / Q000503:physiopathology / Q000628:therapy; D019194:Ischemic Preconditioning; D000066829:Neuroprotection / Q000502:physiology*
keywords: Endogenous protection; Molecular mechanisms; Preconditioning; Stroke; Tissue tolerance