Uncoupling the CRMP2-Ca_V2.2 Interaction Reduces Pain-Like Behavior in a Preclinical Joint-Pain Model.

ABSTRACT: Osteoarthritis (OA) represents a significant pain challenge globally, as current treatments are limited and come with substantial and adverse side effects. Voltage-gated calcium channels have proved to be pharmacologically effective targets, with multiple Food and Drug Administration-approved Ca_V2.2 modulators available for the treatment of pain. Although effective, drugs targeting Ca_V2.2 are complicated by the same obstacles facing other pain therapeutics-invasive routes of administration, narrow therapeutic windows, side effects, and addiction potential. We have identified a key regulator of Ca_V2.2 channels, collapsin response mediator protein 2, that allows us to indirectly regulate Ca_V2.2 expression and function. We previously developed a pep

SUBMITTER: Allen HN 

PROVIDER: S-EPMC11560641 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature