ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 82 citations in OpenAlex.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- TGF-β-induced autophagy in pulmonary artery endothelial cells associated with chronic thromboembolic pulmonary hypertension.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026Review
- The Interplay Between Pulmonary Hypertension and Atrial Fibrillation: A Comprehensive Overview.Cells · 2025Review
- Understanding the molecular regulatory mechanisms of autophagy in lung disease pathogenesis.Frontiers in immunology · 2024Review
- Cell Death in Pulmonary Arterial Hypertension.International journal of medical sciences · 2024Review
- E-cigarettes Induce Dysregulation of Autophagy Leading to Endothelial Dysfunction in Pulmonary Arterial Hypertension.Stem cells (Dayton, Ohio) · 2023Article
- Farnesyl diphosphate synthase regulated endothelial proliferation and autophagy during rat pulmonary arterial hypertension induced by monocrotaline.Molecular medicine (Cambridge, Mass.) · 2022Article
- FUNDC1-mediated mitophagy and HIF1α activation drives pulmonary hypertension during hypoxia.Cell death & disease · 2022Article
- LncRNA-GAS5/miR-382-3p axis inhibits pulmonary artery remodeling and promotes autophagy in chronic thromboembolic pulmonary hypertension.Genes & genomics · 2022Article
- Mitochondrial dysfunction in pulmonary arterial hypertension.Frontiers in physiology · 2022Review
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
- Nitric Oxide-cGMP Pathway Modulation in an Experimental Model of Hypoxic Pulmonary Hypertension.Journal of cardiovascular pharmacology and therapeutics · 2021Article
- Targeting Oxidative Stress as a Therapeutic Approach for Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2021Review
- Beclin-1-Dependent Autophagy Improves Outcomes of Pneumonia-Induced Sepsis.Frontiers in cellular and infection microbiology · 2021Article
- Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.Redox biology · 2020Review
- Article
- NADPH oxidases: Pathophysiology and therapeutic potential in age-associated pulmonary fibrosis.Redox biology · 2020Review
- Mitophagy in Cardiovascular Diseases.Journal of clinical medicine · 2020Review
- Autophagy, Unfolded Protein Response and Lung Disease.Current research in cell biology · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Autophagy is a process for cells to degrade proteins or entire organelles to maintain a balance in the synthesis, degradation, and subsequent recycling of cellular products. Increased reactive oxygen species formation is known to induce autophagy. We previously reported that increased NADPH oxidase (NOX) activity in pulmonary artery endothelial cells (PAEC) from fetal lambs with persistent pulmonary hypertension (PPHN) contributes to impaired angiogenesis in PPHN-PAEC compared with normal PAEC. We hypothesized that increased NOX activity in PPHN-PAEC is associated with increased autophagy, which, in turn, contributes to impaired angiogenesis in PPHN-PAEC. In the present study, we detected increased autophagy in PPHN-PAEC as shown by increased ratio of the microtubule-associated protein 1 light chain (LC3)-II to LC3-I and increased percentage of green fluorescent protein-LC3 punctate positive cells. Inhibiting autophagy by 3-methyladenine, chloroquine, and beclin-1 knockdown in PPHN-PAEC has led to decreased autophagy and increased in vitro angiogenesis. Inhibition of autophagy also decreased the association between gp91(phox) and p47(phox), NOX activity, and superoxide generation. A nonspecific antioxidant N-acetylcysteine and a NOX inhibitor apocynin decreased autophagy in PPHN-PAEC. In conclusion, autophagy may contribute to impaired angiogenesis in PPHN-PAEC through increasing NOX activity. Our results suggest that, in PPHN-PAEC, a positive feedback relationship between autophagy and NOX activity may regulate angiogenesis.
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