p66(shc)'s role as an essential mitophagic molecule in controlling neuronal redox and energetic tone.
Stroke is the leading cause of adult disability in the U.S. and is now recognized as a global epidemic. There are currently no FDA-approved drugs to block the cell death that results from oxygen and glucose deprivation. This void in clinical medicine has sparked an intense interest in understanding endogenous cellular protective pathways that might be exploited for therapeutic development. The work highlighted here describes the critical role between redox tone and energetic stress signaling in mediating mitophagy and determining neuronal cell fate following acute oxygen glucose deprivation.
Kleman
Amy M
AM
Neuroscience Graduate Program, Vanderbilt University, Nashville, TN, USA.
Brown
Jacquelynn E
JE
Zeiger
Stephanie L H
SL
Hettinger
Jane C
JC
Brooks
Joshua D
JD
Holt
Benjamin
B
Morrow
Jason D
JD
Musiek
Erik S
ES
Milne
Ginger L
GL
McLaughlin
BethAnn
B
D000328:Adult; D001343:Autophagy / Q000502:physiology*; D002478:Cells, Cultured; D006801:Humans; D019194:Ischemic Preconditioning; D008928:Mitochondria / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure*; D010084:Oxidation-Reduction; D011494:Protein Kinases / Q000378:metabolism; D055765:Shc Signaling Adaptor Proteins / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D020521:Stroke / Q000473:pathology / Q000503:physiopathology
C528024:SHC1 protein, human; D055765:Shc Signaling Adaptor Proteins; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D011494:Protein Kinases