ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Hypoxia inhibits expression and function of mitochondrial thioredoxin 2 to promote pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026Review
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Puerarin-V prevents the progression of hypoxia- and monocrotaline-induced pulmonary hypertension in rodent models.Acta pharmacologica Sinica · 2022Article
- Blueberry extract improves redox balance and functional parameters in the right ventricle from rats with pulmonary arterial hypertension.European journal of nutrition · 2022Article
- Review
- Transcriptomic analysis identifies Toll-like and Nod-like pathways and necroptosis in pulmonary arterial hypertension.Journal of cellular and molecular medicine · 2020Article
- Protein tyrosine phosphatase L1 represses endothelial-mesenchymal transition by inhibiting IL-1β/NF-κB/Snail signaling.Acta pharmacologica Sinica · 2020Article
- MiR-4463 inhibits the migration of human aortic smooth muscle cells by AMOT.Bioscience reports · 2018Article
- Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Review on Chamber-Specific Differences in Right and Left Heart Reactive Oxygen Species Handling.Frontiers in physiology · 2018Article
- Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2017Review
- The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk.Antioxidants (Basel, Switzerland) · 2017Review
- Hypoxia-induced alterations in the lung ubiquitin proteasome system during pulmonary hypertension pathogenesis.Pulmonary circulationArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance, pulmonary vascular remodeling, and increased pulmonary vascular pressures that often result in right ventricular dysfunction, leading to right heart failure. Evidence suggests that reactive oxygen species (ROS) contribute to PH pathogenesis by altering pulmonary vascular cell proliferation and intracellular signaling pathways. However, the role of mitochondrial antioxidants and oxidant-derived stress signaling in the development of hypoxia-induced PH is largely unknown. Therefore, we examined the role of the major mitochondrial redox regulator thioredoxin 2 (Trx2). Levels of Trx2 mRNA and protein were examined in human pulmonary arterial endothelial cells (HPAECs) and smooth muscle cells (HPASMCs) exposed to hypoxia, a common stimulus for PH, for 72 h. Hypoxia decreased Trx2 mRNA and protein levels. In vitro overexpression of Trx2 reduced hypoxia-induced H
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