Biological Functions and Therapeutic Potential of Autophagy in Spinal Cord Injury

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.

DADLE promotes motor function recovery by inhibiting cytosolic phospholipase A2 mediated lysosomal membrane permeabilization after spinal cord injury

“…Autophagy, a lysosome-based degradation process, is evolutionarily conserved and plays a critical role in diverse pathophysiological conditions across various environments. (Liao et al, 2021). Necroptosis is a regulated form of necrosis mediated by RIPK1 and RIPK3 that is capable of exacerbating cell death and neuroinflammation in the pathogenesis of central nervous system diseases (Fan et al, 2019;Liu et al, 2018).…”

Oxymatrine and insulin resistance: Focusing on mechanistic intricacies involve in diabetes associated cardiomyopathy via SIRT1/AMPK and TGF‐β signaling pathway

“…[ 76 ] Moreover, study of Li et al indicate that treatment with oxymatrine of rats with spinal cord injuriessignificantly ameliorates apoptosis and regulates autophagy, which aremediated by activation of the AMPK/SIRT1 signaling pathway. [ 77 ] Additionally, findings of numerous research studies have indicated that oxymatrine can increase the expression of AMPK, and it is well known to regulatemetabolism, oxidative stress, inflammation, and apoptosis in diabetic conditions, which may attenuate, and could play a promising role in the complications of hyperglycemia‐induced ventricular hypertrophy, cardiac fibrosis, contractile dysfunction, and heart failure.…”

Main Cations and Cellular Biology of Traumatic Spinal Cord Injury

“…Lithium has been shown to inhibit multiple phosphomonoesterases being structurally similar to magnesium [ 89 ]. Lithium can improve the microenvironment in the spinal cord and promote the regeneration and survival of motor neurons [ 90 ]. Lithium chloride can boost the secretion of brain-derived neurotrophic factor (BDNF) in the axons of motor neurons following spinal cord injury [ 91 , 92 ].…”