The role of purinergic receptors in neural repair and regeneration after spinal cord injury

Abstract

Spinal cord injury is a serious injury of the central nervous system that results in neurological deficits. The pathophysiological mechanisms underlying spinal cord injury, as well as the mechanisms involved in neural repair and regeneration, are highly complex. Although there have been many studies on these mechanisms, there is no effective intervention for such injury. In spinal cord injury, neural repair and regeneration is an important part of improving neurological function after injury, although the low regenerative ability of nerve cells and the difficulty in axonal and myelin regeneration after spinal cord injury hamper functional recovery. Large amounts of ATP and its metabolites are released after spinal cord injury and participate in various aspects of functional regulation by acting on purinergic receptors which are widely expressed in the spinal cord. These processes mediate intracellular and extracellular signalling pathways to improve neural repair and regeneration after spinal cord injury. This article reviews research on the mechanistic roles of purinergic receptors in spinal cord injury, highlighting the potential role of purinergic receptors as interventional targets for neural repair and regeneration after spinal cord injury.

Acetyl‐11‐keto‐beta‐boswellic acid modulates macrophage polarization and Schwann cell migration to accelerate spinal cord injury repair in rats

“…50 Schwann cells are most likely involved in endogenous repair after spinal cord injury. 13 Our previous studies have shown that AKBA can promote the expression of BDNF and NGF. 24 The results of this experiment…”

“…11 Therefore, the migration of Schwann cells contributes to the repair of spinal cord injury. 12,13 Reactive oxygen species (ROS) are signaling molecules essential for the progression of the immune response, 14 and nuclear factor E2related factor 2 (Nrf2) is a key nuclear factor in the cellular defense mechanism against oxidative stress, activating downstream antioxidant enzymes such as heme oxygenase 1 (HO-1) to protect cells from oxidative damage and inflammation generated by ROS stimulation. 15 It has been shown that Nrf2 plays a key role in the immune system, limiting the inflammatory response by inhibiting ROS and the pro-inflammatory cytokines IL-1β, and IL-6.…”

P2X7 receptor activation awakes a dormant stem cell niche in the adult spinal cord

“…However, the mechanisms that trigger the resumption of the proliferation of ependymal cells and the migration of their progeny are unknown. ATP is one of various “alarmins” released immediately after tissue injury ( Gadani et al, 2015 ) and has been involved as an important signaling molecule after SCI ( Cotrina and Nedergaard, 2009 ; Cheng et al, 2023 ). We show here that the activation of P2X7r plays a major part in the reactivation of the ependymal stem cell niche mimicking some of the phenomenology elicited by SCI in ependymal cells.…”

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

“…It functions by binding to the Nogo‐66 receptor (NgR) on the surface of neurons, thereby inhibiting neuronal growth and synaptic plasticity, helping establish stable connections in the nervous system. However, following damage to the nervous system, the inhibitory effect of Nogo‐A on neuronal regeneration and synaptic plasticity can hinder nervous system repair (Chambel & Cruz, 2023; Metzdorf et al., 2021; Rust et al., 2019; Schwab & Strittmatter, 2014; Wang et al., 2012) (Figure 1b) (Table 10).…”