Neuronal and endothelial transglutaminase-2 expression in experimental autoimmune encephalomyelitis and multiple sclerosis
Damien D.Pearse1
Mousumi Ghosh2
1.Miami Project to Cure Paralysis,University of Miami Miller School of Medicine,Miami,FL,USA;Department of Neurological Surgery,University of Miami Miller School of Medicine,Miami,FL,USA;Neuroscience Program,Interdisciplinary Stem Cell Institute,University of Miami Miller School of Medicine,Miami,FL,USA;Department of Veterans Affairs,Veterans Affairs Medical Center,Miami,FL,USA2.Miami Project to Cure Paralysis,University of Miami Miller School of Medicine,Miami,FL,USA;Department of Neurological Surgery,University of Miami Miller School of Medicine,Miami,FL,USA;Department of Veterans Affairs,Veterans Affairs Medical Center,Miami,FL,USA
摘要：Multiple sclerosis (MS) is a neurological condition characterized by the disruption of the blood-brain barrier, immune system activation, and inflammation that is accompanied by glial reactivity, neuronal cell death, axon demyelination, and axotomy. Pathological changes result in functional loss including paralysis, migraine, vision problems, spasticity, and neuropathic pain. Although the causative factor responsible for triggering MS remains to be identified, anti-inflammatory treatments have been translated to clinical use with favorable reductions in the frequency, severity, and duration of relapses in the relapsing-remitting form of MS. Among the identified therapeutic targets in MS, transglutaminase-2 (TG2) has been reported to be involved in disease pathogenesis (Chrobok et al., 2018).
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论文发表日期：2022-07-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1471-1472 )