Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy. - Wikidata - awgldk - TriplyDB

Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

http://www.wikidata.org/entity/Q36631660

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Aldose reductase inhibitors for the treatment of diabetic polyneuropathy Olesoxime (cholest-4-en-3-one, oxime): analgesic and neuroprotective effects in a rat model of painful peripheral neuropathy produced by the chemotherapeutic agent, paclitaxel Mitochondria in the pathogenesis of diabetes: a proteomic view Neurotoxic catecholamine metabolite in nociceptors contributes to painful peripheral neuropathy Targeting neuroprotection as an alternative approach to preventing and treating neuropathic pain Diabetic neuropathy: mechanisms to management Global transcriptional programs in peripheral nerve endoneurium and DRG are resistant to the onset of type 1 diabetic neuropathy in Ins2 mice.Transient Receptor Potential Vanilloid 1 is essential for cisplatin-induced heat hyperalgesia in mice Measurement of DCF fluorescence as a measure of reactive oxygen species in murine islets of Langerhans The cytosolic domain of Fis1 binds and reversibly clusters lipid vesicles.Puerarin prevents high glucose-induced apoptosis of Schwann cells by inhibiting oxidative stress.Mechanisms of disease: the oxidative stress theory of diabetic neuropathy Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves.Direct binding of the dynamin-like GTPase, Dnm1, to mitochondrial dynamics protein Fis1 is negatively regulated by the Fis1 N-terminal arm Ginsenoside Rb1 relieves glucose fluctuation-induced oxidative stress and apoptosis in Schwann cells.Mitochondrial configurations in peripheral nerve suggest differential ATP production.Transient receptor potential channels: targeting pain at the source.Context-Dependent Role of Mitochondrial Fusion-Fission in Clonal Expansion of mtDNA Mutations Fisetin Imparts Neuroprotection in Experimental Diabetic Neuropathy by Modulating Nrf2 and NF-κB Pathways.Neurodegeneration and early lethality in superoxide dismutase 2-deficient mice: a comprehensive analysis of the central and peripheral nervous systems Identification of biomarkers for type 2 diabetes and its complications: a bioinformatic approach.Pathogenesis of diabetic neuropathy: bad to the bone.Aquaporin 11 insufficiency modulates kidney susceptibility to oxidative stress.Potential Therapeutic Benefits of Maintaining Mitochondrial Health in Peripheral Neuropathies.Bone marrow mononuclear cells have neurovascular tropism and improve diabetic neuropathy.High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy.Cardiac autonomic neuropathy in patients with diabetes mellitus.Dorsal Root Ganglia Sensory Neuronal Cultures: a tool for drug discovery for peripheral neuropathies.Cisplatin : an old drug with a newfound efficacy -- from mechanisms of action to cytotoxicity.Mechanism of diabetic neuropathy: Where are we now and where to go?New insights in (inter)cellular mechanisms by heart failure with preserved ejection fraction.Brain alterations and clinical symptoms of dementia in diabetes: aβ/tau-dependent and independent mechanisms.Mitochondrial DNA (mtDNA) biogenesis: visualization and duel incorporation of BrdU and EdU into newly synthesized mtDNA in vitro.Evaluation of Cisplatin Neurotoxicity in Cultured Rat Dorsal Root Ganglia via Cytosolic Calcium Accumulation.Selective responses of myenteric neurons to oxidative stress and diabetic stimuli.The Role of Oxidative Stress, Mitochondrial Function, and Autophagy in Diabetic Polyneuropathy.Altered Mitochondrial Anatomy of Trigeminal Ganglia Neurons in Diabetes.Three-dimensional Imaging and Analysis of Mitochondria within Human Intraepidermal Nerve Fibers.Anti-inflammatory effect of AMPK signaling pathway in rat model of diabetic neuropathy.Extracellular Sphingomyelinase Rv0888 of Mycobacterium tuberculosis Contributes to Pathological Lung Injury of Mycobacterium smegmatis in Mice via Inducing Formation of Neutrophil Extracellular Traps.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

http://www.wikidata.org/entity/Q36631660

description

2006 nî lūn-bûn

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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2006年论文

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2006年论文

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name

Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Nature Clinical Practice Neurology

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Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.

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Eva L Feldman

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Gina M Leinninger

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James L Edwards

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Matthew J Lipshaw

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P2860

Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria

Identification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosis

Quantitation of mitochondrial dynamics by photolabeling of individual organelles shows that mitochondrial fusion is blocked during the Bax activation phase of apoptosis

Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis

Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosis

Oxidative stress-induced apoptosis in neurons correlates with mitochondrial DNA base excision repair pathway imbalance.

Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group

The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group

Biochemistry and molecular cell biology of diabetic complications

Nuclear gene OPA1, encoding a mitochondrial dynamin-related protein, is mutated in dominant optic atrophy

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620-628

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10.1038/NCPNEURO0320

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11

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2

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17057749

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