Cell death in the injured brain: Roles of metallothioneins

Article ID	Journal	Published Year	Pages	File Type
2019023	Progress in Histochemistry and Cytochemistry	2009	27 Pages	PDF

Abstract

This paper provides an overview of the TBI pathophysiology leading to cell death and neurological impairment. We also discuss endogenously expressed neuroprotectants and drug candidates, which at this stage may still hold the potential for treating brain injured patients.

Keywords

RAIDD p53-upregulated modulator of apoptosis phorbol-12-myristate-13-acetate-induced protein 1 PBN FGF Bcl-2 SVZ iNOS FADD APAf-1 tumor necrosis factor-like weak inducer of apoptosis MDA PARP AMPA ATG TBI ADP N-methyl-d-aspartate EAE NGF GDNF NMDA PSA-NCAM NSC PIDD PI3K HSC MMP TWEAK LTα TNFα ICAM LC-3 CMA GFAP damage-regulated autophagy modulator PCD mTOR DRAM PKB TGFβ Chaperone-mediated autophagy BDNF BH3 Interacting Domain Death Agonist ROS adenosine diphosphate Traumatic brain injury experimental autoimmune encephalomyelitis AIF Noxa interleukin Bax transforming growth factor-beta TRAMP tumor necrosis factor-alpha TUNEL Fas-associated death domain CNS microtubule-associated protein light chain 3 BBB Blood–brain barrier Neural stem cell inducible nitric oxide synthase central nervous system heat shock cognate Apoptotic protease-activating factor 1 apoptosis-inducing factor Fas Ligand FasL Vascular endothelial growth factor Vascular Endothelial Growth Factor (VEGF)nerve growth factor fibroblast growth factor Glial cell line-derived neurotrophic factor Brain-derived neurotrophic factor phosphoinositide 3 kinase lymphotoxin-α malondialdehyde MOMP Metallothionein Matrix metalloproteinases Programmed cell death subventricular zone wild-type mice intercellular adhesion molecule Mac-1 Neurotrophin nitrotyrosine mammalian target of rapamycin RIP Bcl-2-associated X protein Glial fibrillary acidic protein Ribosome-inactivating protein protein kinase B BAK poly(ADP-ribose)polymerase PUMA BID Reactive oxygen species