Abstract
Chronic pain has been widely recognized as a major public health problem that impacts multiple aspects of patient quality of life. Unfortunately, chronic pain is often resistant to conventional analgesics, which are further limited by their various side effects. New therapeutic strategies and targets are needed to better serve the millions of people suffering from this devastating disease. To this end, recent clinical and preclinical studies have implicated the epidermal growth factor receptor signaling pathway in chronic pain states. EGFR is one of four members of the ErbB family of receptor tyrosine kinases that have key roles in development and the progression of many cancers. EGFR functions by activating many intracellular signaling pathways following binding of various ligands to the receptor. Several of these signaling pathways, such as phosphatidylinositol 3-kinase, are known mediators of pain. EGFR inhibitors are known for their use as cancer therapeutics but given recent evidence in pilot clinical and preclinical investigations, may have clinical use for treating chronic pain. Here, we review the clinical and preclinical evidence implicating EGFR in pathological pain states and provide an overview of EGFR signaling highlighting how EGFR and its ligands drive pain hypersensitivity and interact with important pain pathways such as the opioid system.
Highlights
Chronic pain is an international health priority (Kamerman et al, 2015), with a prevalence approaching 30% in North American adults (Moulin et al, 2002; Johannes et al, 2010)
epidermal growth factor receptor (EGFR) in Pathological Pain neuropathic pain is often resistant to standard analgesics, which are further limited by a variety of adverse side effects (Colloca et al, 2017; Cavalli et al, 2019)
A recent report has shown that gefitinib administration does not block spinal nerve ligation (SNL)-induced mechanical allodynia, though the authors suggest that the discrepancy between this and previous findings may be due to differences in spared nerve injury (SNI) and SNL models of neuropathic pain (Puig et al, 2020)
Summary
Chronic pain is an international health priority (Kamerman et al, 2015), with a prevalence approaching 30% in North American adults (Moulin et al, 2002; Johannes et al, 2010). Recent clinical and preclinical studies have implicated the epidermal growth factor receptor signaling pathway in chronic pain states. A recent report has shown that gefitinib administration does not block spinal nerve ligation (SNL)-induced mechanical allodynia, though the authors suggest that the discrepancy between this and previous findings may be due to differences in SNI and SNL models of neuropathic pain (Puig et al, 2020).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
