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• W1920905062 startingPage "245" @default.
• W1920905062 abstract "Chronic obstructive pulmonary disease (COPD) affect millions of people worldwide and is known to be one of the leading causes of death. The highly sensitive airways protect themselves from irritants by cough and sneeze which propel endogenous and exogenous substances to minimize airway noxious effects. One noxious effect of these substances is activation of peripheral sensory nerve endings of nociceptor neurons innervating these airways lining thus transmitting dangerous signals from the environment to the central nervous system (CNS). Nociceptor neurons include transient receptor potential (TRP) ion channels, especially the vanilloid and ankyrin subfamilies, TRPV1/A1 which can be activated by noxious chemical challenges in models of airways disease. As oxidative stress may activate airways sensory neurons and contribute to COPD exacerbations we sought to review the role that TRP channel activation by oxidative signals may have on airway responses. i0 t would be prudent to target the TRP channels with antagonists and lower systemic oxidative stress with agents that can modulate TRP expression and boost the endogenous levels of antioxidants for treatment and management of COPD." @default.
• W1920905062 created "2016-06-24" @default.
• W1920905062 creator A5014867543 @default.
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• W1920905062 creator A5069400840 @default.
• W1920905062 date "2015-01-01" @default.
• W1920905062 modified "2023-09-26" @default.
• W1920905062 title "Role of oxidative stress & transient receptor potential in chronic obstructive pulmonary disease" @default.
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• W1920905062 doi "https://doi.org/10.4103/0971-5916.166529" @default.
• W1920905062 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4669859" @default.
• W1920905062 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26458340" @default.
• W1920905062 hasPublicationYear "2015" @default.
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