NADPH oxidase subunit NOXO1 is a target for emphysema treatment in COPD.
Michael SeimetzNatascha SommerMariola BednorzOleg PakChristine VeithStefan HadzicMarija GredicNirmal ParajuliBaktybek KojonazarovSimone KrautJochen WilhelmFenja KnoeppIngrid HennekeAlexandra PichlZeki I KanbagliSusan ScheibeAthanasios FysikopoulosCheng-Yu WuWalter KlepetkoPeter JakschChristina A EichstaedtEkkehard GrünigKatrin HinderhoferMiklós GeisztNiklas MüllerFlavia RezendeGiulia Karolin BuchmannIlka WittigMatthias HeckerAndreas HeckerWinfried PadbergPeter DorfmüllerStefan GattenlöhnerClaus F VogelmeierAndreas GüntherSrikanth KarnatiEveline Baumgart-VogtRalph Theo SchermulyHossein Ardeschir GhofraniHorst-Walter BirkKatrin SchroderFriedrich GrimmingerRalf P BrandesNorbert WeissmannPublished in: Nature metabolism (2020)
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and death worldwide. Peroxynitrite, formed from nitric oxide, which is derived from inducible nitric oxide synthase, and superoxide, has been implicated in the development of emphysema, but the source of the superoxide was hitherto not characterized. Here, we identify the non-phagocytic NADPH oxidase organizer 1 (NOXO1) as the superoxide source and an essential driver of smoke-induced emphysema and pulmonary hypertension development in mice. NOXO1 is consistently upregulated in two models of lung emphysema, Cybb (also known as NADPH oxidase 2, Nox2)-knockout mice and wild-type mice with tobacco-smoke-induced emphysema, and in human COPD. Noxo1-knockout mice are protected against tobacco-smoke-induced pulmonary hypertension and emphysema. Quantification of superoxide, nitrotyrosine and multiple NOXO1-dependent signalling pathways confirm that peroxynitrite formation from nitric oxide and superoxide is a driver of lung emphysema. Our results suggest that NOXO1 may have potential as a therapeutic target in emphysema.
Keyphrases
- chronic obstructive pulmonary disease
- lung function
- nitric oxide
- hydrogen peroxide
- nitric oxide synthase
- pulmonary hypertension
- high glucose
- wild type
- pulmonary fibrosis
- cystic fibrosis
- diabetic rats
- endothelial cells
- drug induced
- pulmonary artery
- type diabetes
- oxidative stress
- living cells
- reactive oxygen species
- climate change
- replacement therapy