| Literature DB >> 28110083 |
Sijie Li1, Adam Hafeez2, Fatima Noorulla2, Xiaokun Geng3, Guo Shao4, Changhong Ren4, Guowei Lu4, Heng Zhao5, Yuchuan Ding6, Xunming Ji7.
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.Entities:
Keywords: Endogenous protection; Molecular mechanisms; Preconditioning; Stroke; Tissue tolerance
Mesh:
Year: 2017 PMID: 28110083 PMCID: PMC5515698 DOI: 10.1016/j.pneurobio.2017.01.001
Source DB: PubMed Journal: Prog Neurobiol ISSN: 0301-0082 Impact factor: 11.685