Academic Journal
Pathological roles of transient receptor potential channels in chronic obstructive pulmonary disease: special focus on cellular mechanisms.
| Τίτλος: | Pathological roles of transient receptor potential channels in chronic obstructive pulmonary disease: special focus on cellular mechanisms. |
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| Συγγραφείς: | Ye YR; School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China., Zhou YY; School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China., Qu S; School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China., Zhou WL; School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China., Chen L; State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital, Guangzhou Medical University, Guangzhou, P. R. China., Zhang YL; School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China.; Guangdong Engineering and Technology Research Center for Quality and Efficacy Re-evaluation of Post-marketed TCM, Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, School of Life Sciences, Sun Yat-Sen University, Guangzhou, P. R. China. |
| Πηγή: | Expert review of respiratory medicine [Expert Rev Respir Med] 2026 Aug; Vol. 20 (8), pp. 953-962. Date of Electronic Publication: 2026 Mar 30. |
| Τύπος έκδοσης: | Journal Article; Review |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Taylor & Francis Country of Publication: England NLM ID: 101278196 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1747-6356 (Electronic) Linking ISSN: 17476348 NLM ISO Abbreviation: Expert Rev Respir Med Subsets: MEDLINE |
| Imprint Name(s): | Publication: 2015- : Abingdon, Oxford : Taylor & Francis Original Publication: London : Future Drugs, c2007- |
| Ιατρικοί όροι (MeSH): | Pulmonary Disease, Chronic Obstructive*/physiopathology , Pulmonary Disease, Chronic Obstructive*/drug therapy , Transient Receptor Potential Channels*/metabolism, Humans ; Animals |
| Περίληψη: | Introduction: Transient receptor potential (TRP) channels comprise a superfamily of cation-permeable channels broadly expressed in the respiratory tract, playing essential roles in regulating epithelial integrity, mucus secretion, mechanotransduction, and innate immune responses. Increasing evidence suggests that dysregulation of TRP channels contributes to the pathogenesis of chronic obstructive pulmonary disease (COPD). Areas Covered: This review summarizes current insights into the cellular mechanisms by which TRP channels contribute to COPD, with particular emphasis on respiratory epithelial dysfunction while also incorporating selected non-epithelial mechanisms relevant to disease pathogenesis. A comprehensive literature search was conducted in PubMed and Web of Science up to January 2026. Expert Opinion: Evidence for TRP involvement in COPD is heterogeneous. TRPV4 currently has the strongest mechanistic and translational support, whereas TRPC1 and TRPC6 still require further therapeutic validation. TRPV2 appears to be linked more specifically to macrophage dysfunction and emphysema-related pathology, whereas the roles of TRPV6 and TRPM6 are still incompletely defined. 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, while safety concerns also remain. Future progress will require COPD-specific validation, localized delivery, and biomarker-guided treatment strategies matched to defined disease phenotypes. |
| Contributed Indexing: | Keywords: Airway epithelium; cellular mechanisms; chronic obstructive pulmonary disease; ion channel; transient receptor potential channels |
| Substance Nomenclature: | 0 (Transient Receptor Potential Channels) |
| Entry Date(s): | Date Created: 20260326 Date Completed: 20260803 Latest Revision: 20260803 |
| Update Code: | 20260803 |
| DOI: | 10.1080/17476348.2026.2652117 |
| PMID: | 41886309 |
| Βάση Δεδομένων: | MEDLINE |
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