Abstract
Previous studies have indicated that autophagy plays a critical role in spinal cord injury (SCI), including traumatic spinal cord injury (TSCI) and ischemia-reperfusion spinal cord injury (IRSCI). However, while the understanding of mechanisms underlying autophagy in SCI has progressed, there remain several controversial points: (1) temporal pattern results of autophagic activation after SCI are not consistent across studies; (2) effect of accumulation of autophagosomes due to the blockade or enhancement of autophagic flux is uncertain; (3) overall effect of enhanced autophagy remains undefined, with both beneficial and detrimental outcomes reported in SCI literature. In this review, the temporal pattern of autophagic activation, autophagic flux, autophagic cell death, relationship between autophagy and apoptosis, and pharmacological intervention of autophagy in TSCI (contusion injury, compression injury and hemisection injury) and IRSCI are discussed. Types of SCI and severity appear to contribute to differences in outcomes regarding temporal pattern, flux, and function of autophagy. With future development of specific strategies on autophagy intervention, autophagy may play an important role in improving functional recovery in patients with SCI.
Highlights
Spinal cord injury (SCI) is a major disabling disease currently with insufficient treatment options
Types of spinal cord injury (SCI) and severity may contribute to the differences in outcomes regarding temporal pattern, activation, and function of autophagy
The situation of autophagic flux may depend on the injury severity in SCI, where severe injury results in the blockade of flux, and moderate injury causes the enhancement of flux after SCI
Summary
Spinal cord injury (SCI) is a major disabling disease currently with insufficient treatment options. Though it is widely accepted that autophagy plays a critical role in spinal cord injuries, recent exploration and studies revealed several controversial points: (1) temporal pattern results of autophagic activation after SCI are not consistent across studies; (2) effect of accumulation of autophagosomes due to the blockade or enhancement of autophagic flux is uncertain; and (3) overall effect of increased autophagy remains undefined, with both beneficial and detrimental outcomes reported in literature. Among these models, hemisection injury, contuSstiuodnieinsjuabryo,uatntdhecotemmpproesrasilopnaitntejurnryoaf raeumtoopshtafgreicqaucetnivtlaytiuosnedin, eSsCpIeacriaelfluynindathmeeanutatol panhdagcircuScCiaIl. eTxhpeeyrimareentbaelnreefsiecaiarcl hfo[2r7,u2n8d,4e4r]s.tanding progress of autophagy and its relationships with other pathologic events, and choosing appropriate time points for autophagic regulation after SCI. Hemisection injury, contuSstiuodnieinsjuabryo,uatntdhecotemmpproesrasilopnaitntejurnryoaf raeumtoopshtafgreicqaucetnivtlaytiuosnedin, eSsCpIeacriaelfluynindathmeeanutatol panhdagcircuScCiaIl. eTxhpeeyrimareentbaelnreefsiecaiarcl hfo[2r7,u2n8d,4e4r]s.tanding progress of autophagy and its relationships with other pathologic events, and choosing appropriate time points for autophagic regulation after SCI Results from these studies are not consistent. These results are represented for TSCI and IRSCI as follows
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