Exploring the molecular pathways and therapeutic implications of angiogenesis in neuropathic pain

Recently, much attention has been paid to chronic neuro-inflammatory condition underlying neuropathic pain. It is generally linked with thermal hyperalgesia and tactile allodynia. It results due to injury or infection in the nervous system. The neuropathic pain spectrum covers a variety of pathophysiological states, mostly involved are ischemic injury viral infections associated neuropathies, chemotherapy-induced peripheral neuropathies, autoimmune disorders, traumatic origin, hereditary neuropathies, inflammatory disorders, and channelopathies. In CNS, angiogenesis is evident in inflammation of neurons and pain in bone cancer. The role of chemokines and cytokines is dualistic; their aggressive secretion produces detrimental effects, leading to neuropathic pain. However, whether the angiogenesis contributes and exists in neuropathic pain remains doubtful. In the present review, we elucidated summary of diverse mechanisms of neuropathic pain associated with angiogenesis. Moreover, an overview of multiple targets that have provided insights on the VEGF signaling, signaling through Tie-1 and Tie-2 receptor, erythropoietin pathway promoting axonal growth are also discussed. Because angio-genesis as a result of these signaling, results in inflammation, we focused on the mechanisms of neuropathic pain. These factors are mainly responsible for the activation of post-traumatic regeneration of the PNS and CNS. Furthermore, we also reviewed synthetic and herbal treatments targeting angiogenesis in neuropathic pain.

Automated summary

Recently, there has been increasing focus on the chronic neuro-inflammatory condition causing neuropathic pain, characterized by thermal hyperalgesia and tactile allodynia, which results from injury or infection in the nervous system. Angiogenesis, chemokines, and cytokines play important roles in the pathophysiology of neuropathic pain, contributing to inflammation and detrimental effects. Various mechanisms, including VEGF signaling, Tie-1 and Tie-2 receptor signaling, and erythropoietin pathway promoting axonal growth, have been identified as potential targets for therapeutic interventions in neuropathic pain associated with angiogenesis. Synthetic and herbal treatments targeting angiogenesis in neuropathic pain have also been explored.