Corrigendum: Purinergic signaling systems across comparative models of spinal cord injury

Abstract

[This corrects the article DOI: 10.4103/1673-5374.338993].

Figure 1

Timeline depicting the secondary cellular injury response following mammalian spinal cord injury. The primary mechanical trauma is exacerbated by prolonged cell death, widespread inflammation, reactive gliosis, and axonal degeneration. These events prevent successful regeneration and limit sensorimotor recovery. Created with BioRender.com with permissions and publication license.

Figure 2

Timeline depicting the secondary cellular injury response following non-mammalian spinal cord injury. The primary mechanical trauma induces transient cell death, controlled inflammation, reactive gliosis, neurogenesis, and axonal regeneration. These events conclude within weeks and facilitate recovery and restoration of locomotor function in non-mammalian vertebrates. Created with BioRender.com with permissions and publication license.

Figure 3

Purinergic signaling within the spinal cord microenvironment during the early injury response. The first several days following mammalian SCI are characterized by widespread cell death, migration of various cell types to the lesion, inflammation, and reactive gliosis. Identified roles for purinergic receptors in these processes is summarized. Created with BioRender.com with permissions and publication license. ADP: adenosine diphosphate; ATP: adenosine triphosphate; CD39: cluster of differentiation 39; Ca²⁺: calcium; CREB: cAMP response element-binding protein; ERK1/2: extracellular signal-regulated kinases 1/2; IL: interleukin; NGF2: nerve growth factor-2; NLRP1/3: NLR family pyrin domain containing 1/3; NT3: neurotrophin-3; STAT3: signal transducer and activator of transcription 3; TNF-α: tumor necrosis factor alpha; UDP: uridine diphosphate; UTP: uridine triphosphate. Created with BioRender.com with permissions and publication license.

Figure 4

Purinergic signaling within the spinal cord microenvironment during the chronic injury response. After the first week following mammalian SCI, reactive astrocytes become scar forming, ependymal and neural progenitor cells fail to undergo injury-induced proliferation and neuronal differentiation, and axons continue to degenerate. Identified and hypothesized roles for purinergic receptors in these processes is summarized. Created with BioRender.com with publication permissions and publication license. ADP: Adenosine diphosphate; Akt: protein kinase B; ATP: adenosine triphosphate; BDNF: brain derived neurotrophic factor; CD39: cluster of differentiation 39; Ca²⁺: calcium; CREB: cAMP response element-binding protein; ERK1/2: extracellular signal-regulated kinases 1/2; IL: interleukin; NGF2: nerve growth factor-2; NLRP1/3: NLR family pyrin domain containing 1/3; NT3: neurotrophin-3; STAT3: signal transducer and activator of transcription 3; TNF-α: tumor necrosis factor alpha; UDP: uridine diphosphate; UTP: uridine triphosphate; Wnt: wingless-related intergration site. Created with BioRender.com with permissions and publication license.