Fusion or Fission: The Destiny of Mitochondria In Traumatic Brain Injury of Different Severities
暂无分享,去创建一个
A. Belli | L. Hill | G. Lazzarino | B. Tavazzi | S. Signoretti | V. Di Pietro | G. Lazzarino | Edoardo Porto | A. M. Amorini
[1] A. Gorgey,et al. Mitochondrial mass and activity as a function of body composition in individuals with spinal cord injury , 2017, Physiological reports.
[2] S. Kannurpatti. Mitochondrial calcium homeostasis: Implications for neurovascular and neurometabolic coupling , 2017, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[3] A. Russell,et al. Increased mitophagy in the skeletal muscle of spinal and bulbar muscular atrophy patients , 2017, Human molecular genetics.
[4] A. Belli,et al. Severity of experimental traumatic brain injury modulates changes in concentrations of cerebral free amino acids , 2016, Journal of cellular and molecular medicine.
[5] T. Sanderson,et al. Mitochondrial dynamics following global cerebral ischemia , 2016, Molecular and Cellular Neuroscience.
[6] A. Voigt,et al. The mitochondrial kinase PINK1: functions beyond mitophagy , 2016, Journal of neurochemistry.
[7] M. Berry,et al. Mesenchymal stromal cell-mediated neuroprotection and functional preservation of retinal ganglion cells in a rodent model of glaucoma. , 2016, Cytotherapy.
[8] A. Belli,et al. Metabolic, enzymatic and gene involvement in cerebral glucose dysmetabolism after traumatic brain injury. , 2016, Biochimica et biophysica acta.
[9] Jacob S. Young,et al. Sports-related concussions: diagnosis, complications, and current management strategies. , 2016, Neurosurgical focus.
[10] M. Waxham,et al. Altered Mitochondrial Dynamics and TBI Pathophysiology , 2016, Front. Syst. Neurosci..
[11] Shuixiu Xia,et al. Mitochondrial division inhibitor 1 (Mdivi-1) offers neuroprotection through diminishing cell death and improving functional outcome in a mouse model of traumatic brain injury , 2016, Brain Research.
[12] J. Albrecht,et al. Changes in the mitochondrial antioxidant systems in neurodegenerative diseases and acute brain disorders , 2015, Neurochemistry International.
[13] L. Scorrano,et al. The Opa1-Dependent Mitochondrial Cristae Remodeling Pathway Controls Atrophic, Apoptotic, and Ischemic Tissue Damage , 2015, Cell metabolism.
[14] I. Bohovych,et al. Mitochondrial protein quality control: the mechanisms guarding mitochondrial health. , 2015, Antioxidants & redox signaling.
[15] Sung-Cheng Huang,et al. In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging , 2015, Proceedings of the National Academy of Sciences.
[16] M. Yen,et al. Changes in Mitochondrial Morphology and Bioenergetics in Human Lymphoblastoid Cells With Four Novel OPA1 Mutations. , 2015, Investigative ophthalmology & visual science.
[17] T. Schwarz,et al. PINK1- and PARK2-mediated local mitophagy in distal neuronal axons , 2015, Autophagy.
[18] X. Zhuang,et al. Drp1 inhibition attenuates neurotoxicity and dopamine release deficits in vivo , 2014, Nature Communications.
[19] Zhihui Feng,et al. Mitochondrial dysfunction-associated OPA1 cleavage contributes to muscle degeneration: preventative effect of hydroxytyrosol acetate , 2014, Cell Death and Disease.
[20] Xiaodong Wang,et al. Activation of mitochondrial protease OMA1 by Bax and Bak promotes cytochrome c release during apoptosis , 2014, Proceedings of the National Academy of Sciences.
[21] D. Hovda,et al. The New Neurometabolic Cascade of Concussion. , 2014, Neurosurgery.
[22] A. Luft,et al. 3-Nitropropionic Acid-Induced Ischemia Tolerance in the Rat Brain is Mediated by Reduced Metabolic Activity and Cerebral Blood Flow , 2014, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[23] Bennet Omalu,et al. Chronic Traumatic Encephalopathy , 2019, Traumatic Brain Injury.
[24] B. Zhivotovsky,et al. Free radicals in cross talk between autophagy and apoptosis. , 2014, Antioxidants & redox signaling.
[25] Q. Dong,et al. Amelioration of Ischemic Mitochondrial Injury and Bax‐Dependent Outer Membrane Permeabilization by Mdivi‐1 , 2014, CNS neuroscience & therapeutics.
[26] Prashant Mishra,et al. Proteolytic cleavage of Opa1 stimulates mitochondrial inner membrane fusion and couples fusion to oxidative phosphorylation. , 2014, Cell metabolism.
[27] A. Belli,et al. Neuroglobin expression and oxidant/antioxidant balance after graded traumatic brain injury in the rat. , 2014, Free radical biology & medicine.
[28] A. Logan,et al. The Molecular Mechanisms Affecting N-Acetylaspartate Homeostasis Following Experimental Graded Traumatic Brain Injury , 2014, Molecular medicine.
[29] P. Chinnery,et al. Mitochondrial DNA and traumatic brain injury , 2014, Annals of neurology.
[30] M. Alavi,et al. Dominant optic atrophy, OPA1, and mitochondrial quality control: understanding mitochondrial network dynamics , 2013, Molecular Neurodegeneration.
[31] Alexander M van der Bliek,et al. Mechanisms of mitochondrial fission and fusion. , 2013, Cold Spring Harbor perspectives in biology.
[32] L. Martins,et al. Insights into mitochondrial quality control pathways and Parkinson’s disease , 2013, Journal of Molecular Medicine.
[33] D. Chan,et al. Fis1, Mff, MiD49, and MiD51 mediate Drp1 recruitment in mitochondrial fission , 2013, Molecular biology of the cell.
[34] D. Hovda,et al. Potentially neuroprotective gene modulation in an in vitro model of mild traumatic brain injury , 2013, Molecular and Cellular Biochemistry.
[35] L. Scorrano,et al. The antiapoptotic OPA1/Parl couple participates in mitochondrial adaptation to heat shock☆ , 2012, Biochimica et biophysica acta.
[36] G. Cheng,et al. Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies , 2012, British journal of pharmacology.
[37] A. M. van der Bliek,et al. Mitochondrial Fission, Fusion, and Stress , 2012, Science.
[38] L. Scorrano,et al. Optic atrophy 1 mediates mitochondria remodeling and dopaminergic neurodegeneration linked to complex I deficiency , 2012, Cell Death and Differentiation.
[39] Christian Haass,et al. Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences , 2012, The EMBO journal.
[40] E. Rugarli,et al. Mitochondrial quality control: a matter of life and death for neurons , 2012, The EMBO journal.
[41] N. Plesnila,et al. Inhibition of Drp1 provides neuroprotection in vitro and in vivo , 2012, Cell Death and Differentiation.
[42] David S. Park,et al. The Mitochondrial Inner Membrane GTPase, Optic Atrophy 1 (Opa1), Restores Mitochondrial Morphology and Promotes Neuronal Survival following Excitotoxicity* , 2010, The Journal of Biological Chemistry.
[43] G. Lazzarino,et al. Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications. , 2010, Neurosurgical focus.
[44] Antonio Belli,et al. Transcriptomics of traumatic brain injury: gene expression and molecular pathways of different grades of insult in a rat organotypic hippocampal culture model. , 2010, Journal of neurotrauma.
[45] E. Rugarli,et al. Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1 , 2009, The Journal of cell biology.
[46] J. McCaffery,et al. Mitofusins and OPA1 mediate sequential steps in mitochondrial membrane fusion. , 2009, Molecular biology of the cell.
[47] Jean-Claude Martinou,et al. SLP‐2 is required for stress‐induced mitochondrial hyperfusion , 2009, The EMBO journal.
[48] D. Turnbull,et al. Review: Mitochondria and disease progression in multiple sclerosis , 2008, Neuropathology and applied neurobiology.
[49] T. Kuwana,et al. Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization. , 2008, Developmental cell.
[50] Min Wu,et al. Fission and selective fusion govern mitochondrial segregation and elimination by autophagy , 2008, The EMBO journal.
[51] D. Chan,et al. OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L , 2007, The Journal of cell biology.
[52] Antonio Belli,et al. TEMPORAL WINDOW OF METABOLIC BRAIN VULNERABILITY TO CONCUSSIONS: MITOCHONDRIAL‐RELATED IMPAIRMENT—PART I , 2007, Neurosurgery.
[53] L. Scorrano,et al. A cut short to death: Parl and Opa1 in the regulation of mitochondrial morphology and apoptosis , 2007, Cell Death and Differentiation.
[54] S. Duvezin-Caubet,et al. Proteolytic Processing of OPA1 Links Mitochondrial Dysfunction to Alterations in Mitochondrial Morphology* , 2006, Journal of Biological Chemistry.
[55] Sara Cipolat,et al. OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion , 2006, Cell.
[56] K. Mihara,et al. Regulation of mitochondrial morphology through proteolytic cleavage of OPA1 , 2006, The EMBO journal.
[57] R. Youle,et al. Mitochondrial fission in apoptosis , 2005, Nature Reviews Molecular Cell Biology.
[58] A. Marmarou,et al. Cerebral Oxidative Stress and Depression of Energy Metabolism Correlate with Severity of Diffuse Brain Injury in Rats , 2005, Neurosurgery.
[59] Thomas D. Schmittgen,et al. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.
[60] B. Lorenz,et al. Mutation spectrum and splicing variants in the OPA1 gene , 2001, Human Genetics.
[61] D. Hovda,et al. The Neurometabolic Cascade of Concussion. , 2001, Journal of athletic training.
[62] A. Marmarou,et al. A new model of diffuse brain injury in rats. Part II: Morphological characterization. , 1994, Journal of neurosurgery.
[63] A. Marmarou,et al. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. , 1994, Journal of neurosurgery.
[64] K. Guskiewicz,et al. Acute sports-related traumatic brain injury and repetitive concussion. , 2015, Handbook of clinical neurology.
[65] G. Lazzarino,et al. The Relevance of Assessing Cerebral Metabolic Recovery for a Safe Return to Play Following Concussion , 2014 .
[66] J. Gal,et al. Mitochondrial dysfunction in amyotrophic lateral sclerosis. , 2010, Biochimica et biophysica acta.
[67] George Perry,et al. Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. , 2010, Biochimica et biophysica acta.