Двойная роль оси COX-2/PGE2 в множественном склерозе: от патогенеза до фармакологического ингибирования.
Обработка статьи · этапы, ошибки и управление
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История · было → стало
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Al-Dhahi Ahmed Salem, Al-Kuraishy Hayder M, Hussain Nawar R, Fawzy Mohamed N, Alruwaili Mubarak, Waheed Huda J, Al-Gareeb Ali I, Albuhadily Ali K, Batiha Gaber El-Saber
Аннотация
Оригинал публикации
The dual role of the COX-2/PGE2 Axis in multiple sclerosis: From pathogenesis to pharmacological inhibition.
Multiple sclerosis (MS) is a chronic neuroinflammatory and demyelinating disease of the central nervous system (CNS). The cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) axis plays a complex, dual role in its pathogenesis. Although its upregulation typically induces neuroinflammation, oligodendrocyte apoptosis, and demyelination, certain PGE2 receptors (EP2/EP4) can also mediate protective effects. In experimental models, inhibiting COX-2 (using celecoxib or meloxicam) or blocking pro-inflammatory receptors (EP1/EP3) alleviates disease pathology by reducing immune cell infiltration and cytokine production and protecting oligodendrocytes via both COX-2-dependent and independent mechanisms. This review discusses the potential of selectively targeting the detrimental effects of the COX-2/PGE2 axis (such as EP1/EP3 signaling) while preserving protective pathways as a sophisticated therapeutic strategy for MS. However, cardiovascular risks limit the clinical translation of COX-2 inhibitors, necessitating the development of safer, more precise modulation of this pathway.