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تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
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Potential mechanisms linking metabolic, vascular, and neural defects in diabetic neuropathy

Potential mechanisms linking metabolic, vascular, and neural defects in diabetic neuropathy
Initiator Metabolic defect Metabolic mediator Functional mediator Consequence
↑ Glucose Glycation/AGE Protein cross-linking Matrix defects

Endoneurial fibrosis

↓ Neurotrophic SAM
Protein inactivation Receptor-ligand defects ↓ Neurotrophism
NO quenching Vasoconstriction Ischemia/hypoxia
Macrophage activation Cytokines, ↑ TGF

Cytotoxicity*

Endoneurial fibrosis
Free radical formation Oxidative stress Cytotoxicity
Autooxidation Free radical formation Oxidative stress Cytotoxicity*
↑ Sorbitol pathway ↓ NADPH

Oxidative stress ↓

NO synthesis

Cytotoxicity*

Ischemia/hypoxia
NADH/lactate Pseudohypoxia Cytotoxicity*
↑ Glycation (See above) (See above)
↓ Taurine Oxidative stress Cytotoxicity*
↓ MI/↓ PI/↓ PKC

Signal transduction

Eicosanoid defects

↓ Neurotrophism

Ischemia/hypoxia
↑ DAG ↑ PKC Signal transduction Ischemia
FA defects ↑ Free FA ↑ Long-chain acyl-Co's Mitochondrial defects Cytotoxicity
↓ 3-β-dehydrog ↓ GLA Eicosanoid defects Ischemia/hypoxia
↓ Insulin ?↓ GF expression ?IGF/NGF/BDNF/NT3 Neurotrophic factors ↓ Neurotrophism
AGE: advanced glycosylation end-products; BDNF: brain-derived neurotrophic factor; DAG: diacylglycerol; FA: fatty acid; GLA: gamma linoleic acid; IGF: insulin-like growth factors; MI: myoinositol; NO: nitric oxide; PI: phosphoinositide; PKC: protein kinase C; NT3: neurotrophin-3; SAM: substrate adhesion molecules; TGF: transforming growth factor.
* Cytotoxicity of neural, glial, and vascular components of peripheral nerve.
Adapted from: Stevens MJ, Feldman EL, Greene DA. The aetiology of diabetic neuropathy: the combined roles of metabolic and vascular defects. Diabet Med 1995; 12:566.
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