Current opinion in neurology · 2011
Inflammation and axon regeneration.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Benowitz Larry I, Popovich Phillip G
Аннотация
PURPOSE OF REVIEW: The inflammatory response that accompanies neural injury involves multiple cell types and effector molecules with both positive and negative effects. Inflammation is essential for normal regeneration in the peripheral nervous system, and here we review evidence that augmenting inflammation can enhance regeneration in areas of the central nervous system in which it normally does not occur.
RECENT FINDINGS: Within the spinal cord, inflammation enables transplanted sensory neurons to regenerate lengthy axons and enhances the ability of a trophic factor to promote corticospinal tract sprouting. Induction of inflammation in the eye supports survival of retinal ganglion cells and enables them to regenerate injured axons through the optic nerve. These effects are linked to an atypical trophic factor, oncomodulin, along with other, better known molecules. Induction of inflammation within dorsal root ganglia, when combined with other treatments, enables peripheral sensory neurons to regenerate axons into the spinal cord. However, inflammation also has negative effects that impede recovery.
SUMMARY: In light of the importance of inflammation for neural repair, it is important to identify the specific cell types and molecules responsible for the positive and negative effects of inflammation and to develop treatments that tip the balance to favor repair.
RECENT FINDINGS: Within the spinal cord, inflammation enables transplanted sensory neurons to regenerate lengthy axons and enhances the ability of a trophic factor to promote corticospinal tract sprouting. Induction of inflammation in the eye supports survival of retinal ganglion cells and enables them to regenerate injured axons through the optic nerve. These effects are linked to an atypical trophic factor, oncomodulin, along with other, better known molecules. Induction of inflammation within dorsal root ganglia, when combined with other treatments, enables peripheral sensory neurons to regenerate axons into the spinal cord. However, inflammation also has negative effects that impede recovery.
SUMMARY: In light of the importance of inflammation for neural repair, it is important to identify the specific cell types and molecules responsible for the positive and negative effects of inflammation and to develop treatments that tip the balance to favor repair.