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. Author manuscript; available in PMC: 2009 Aug 10.
Published in final edited form as: Curr Respir Med Rev. 2008;4(1):57–68. doi: 10.2174/157339808783497873

Figure 2. Activation of p38 MAPK, NF-κB and PI3K pathway in COPD and possible therapeutic targets.

Figure 2

Cigarette smoke-mediated oxidative stress can result in activation of various kinases [p38 mitogen-activated protein kinase (p38 MAPK), IκB kinase (IKK) and phosphoinositide 3-kinase (PI3K)] leading to release of pro-inflammatory mediators by activating transcription factor NF-κB. A reversible PI3K inhibitor, LY294002, can restore defective HDAC2 expression and activity (possibly restores steroid efficacy) which were shown in the lungs of patients with COPD. Therefore, these kinases would be possibly therapeutic targets although these inhibitors/modifiers of above-mentioned kinases have not yet been proven by appropriate randomized placebo trials.