Abstract
Autophagy is an evolutionarily conserved lysosomal degradation pathway that maintains metabolism and homeostasis by eliminating protein aggregates and damaged organelles. Many studies have reported that autophagy plays an important role in spinal cord injury (SCI). However, the spatiotemporal patterns of autophagy activation after traumatic SCI are contradictory. Most studies show that the activation of autophagy and inhibition of apoptosis have neuroprotective effects on traumatic SCI. However, reports demonstrate that autophagy is strongly associated with distal neuronal death and the impaired functional recovery following traumatic SCI. This article introduces SCI pathophysiology, the physiology and mechanism of autophagy, and our current review on its role in traumatic SCI. We also discuss the interaction between autophagy and apoptosis and the therapeutic effect of activating or inhibiting autophagy in promoting functional recovery. Thus, we aim to provide a theoretical basis for the biological therapy of SCI.
Highlights
Spinal cord injury (SCI) is one of the most important health problems globally, posing a huge challenge to clinical medicine and basic research and imposing a heavy burden on patients and society (Dumont et al, 2001; Gupta et al, 2010; Zhou et al, 2017a)
A recent study showed that the expression of autophagy biomarkers Beclin-1 and LC3B II increased after the injection of VEGF165 in young male Wistar rats with induced traumatic spinal cord injury (SCI)
The activation of autophagy is an important event, and the promotion or inhibition of autophagy may be a promising therapeutic strategy to manage the pathogenesis of traumatic SCI
Summary
Spinal cord injury (SCI) is one of the most important health problems globally, posing a huge challenge to clinical medicine and basic research and imposing a heavy burden on patients and society (Dumont et al, 2001; Gupta et al, 2010; Zhou et al, 2017a). Autophagy is a general term for an evolutionarily conserved, lysosome-based degradation process playing an important role in various pathophysiological environments (Mizushima and Klionsky, 2007; Mizushima and Levine, 2010; Yang and Klionsky, 2010; Mizushima and Komatsu, 2011; Rubinsztein et al, 2012a; Russell et al, 2014; Avin-Wittenberg, 2019) These include starvation as an adaptive response, intracellular proteins and organelles quality control, anti-aging, tumor formation inhibition, and microorganisms’ elimination in cells (Mizushima and Klionsky, 2007; Levine and Kroemer, 2008; Mizushima et al, 2008; Deretic and Levine, 2009). Recent findings on autophagy’s role in SCI, the regulation, and the level of autophagy flux may become a potential new neuroprotective target, providing a new idea for the clinical treatment of SCI
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