Inflammasomes, Inflammation and Neuropathic Pain

Author:

Sharan Lokesh1,Pal Anubrato1,Saha Priya2,Kumar Ashutosh2

Affiliation:

1. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Kolkata 700054, West Bengal, India

2. Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)-SAS Nagar, Mohali, Punjab, 160062, India

Abstract

Inflammasomes such as NOD-like receptor protein 1 (NLRP1), NLRP3, NLR family CARD domain-containing protein 4 (NLRC4) and absent in melanoma 2 (AIM2) are the primary mediators of inflammation and its associated neuropathic pain. These inflammasomes are activated leading to various autoimmune & metabolic disorders, cancer, and other inflammatory diseases. The activation of inflammasomes occurs due to molecular alterations like mitochondrial dysfunction, neuroinflammation, lysosomal damage, oxidative stress, sensitization, and disinhibition, which lead to proinflammatory pathways causing inflammasome-related neuropathic pain. Among these inflammasomes, NLRP3 has been widely studied and proven to be the key player in the development of neuropathy. In this chapter, we have summarized the role of inflammasome and how NLRP3 is involved in neuropathic pain. Therefore, based on the facts available, it has been suggested that focusing on inflammasome activity may be a cutting-edge and successful treatment approach for neuropathic pain. 

Publisher

BENTHAM SCIENCE PUBLISHERS

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