Evidence for TRP involvement in COPD is heterogeneous rather than uniform. TRPV4 currently has the strongest mechanistic and translational support, whereas TRPC1 and TRPC6 remain less mature therapeutic candidates. TRPV2 appears to be linked more specifically to macrophage dysfunction and emphysema-related pathology, whereas the roles of TRPV6 and TRPM6 remain provisional. A key barrier to clinical translation is that numerous TRP-targeted strategies have been developed outside COPD or have shown limited efficacy in the clinical settings tested to date, in addition to safety concerns. Future progress will require COPD-specific validation, localized delivery, and biomarker-guided treatment strategies matched to defined disease phenotypes.
Ye et al. (Thu,) studied this question.