ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Reactive oxygen species induced Ca
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 109 citations in OpenAlex.
- Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026Review
- From development to regeneration: the endothelial interface in lung injury and repair.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Bioenergetics and metabolism of the pulmonary endothelium. Scientific session I: ReSPIRE 2025.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Role of MiR-542-3p/Integrin-Linked Kinase/Myocardin Signaling Axis in Hypoxic Pulmonary Hypertension.Pulmonary circulation · 2025Article
- Review
- Imaging Ca2+ Signals in Small Pulmonary Veins at Physiological Intraluminal Pressures.Journal of visualized experiments : JoVE · 2025Article
- Advances in the Study for Modulators of Transient Receptor Potential Vanilloid (TRPV) Channel Family.Current topics in medicinal chemistry · 2025Review
- Nanotechnology-Fortified Manipulation of Cell CaSmall science · 2024Article
- Fatty acid metabolism promotes TRPV4 activity in lung microvascular endothelial cells in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Review
- Oxidative Stress and Antioxidant Therapy in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Review
- Natural Products for the Treatment of Pulmonary Hypertension: Mechanism, Progress, and Future Opportunities.Current issues in molecular biology · 2023Review
- ABCB5Stem cell research & therapy · 2023Article
- Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets.Frontiers in physiology · 2023Review
- Transpulmonary amino acid metabolism in the sugen hypoxia model of pulmonary hypertension.Pulmonary circulation · 2023Article
- Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a lethal disease characterized by elevations in pulmonary arterial pressure, in part due to formation of occlusive lesions in the distal arterioles of the lung. These complex lesions may comprise multiple cell types, including endothelial cells (ECs). To better understand the molecular mechanisms underlying EC dysfunction in PAH, lung microvascular endothelial cells (MVECs) were isolated from normoxic rats (N-MVECs) and rats subjected to SU5416 plus hypoxia (SuHx), an experimental model of PAH. Compared with N-MVECs, MVECs isolated from SuHx rats (SuHx-MVECs) appeared larger and more spindle shaped morphologically and expressed canonical smooth muscle cell markers smooth muscle-specific α-actin and myosin heavy chain in addition to endothelial markers such as Griffonia simplicifolia and von Willebrand factor. SuHx-MVEC mitochondria were dysfunctional, as evidenced by increased fragmentation/fission, decreased oxidative phosphorylation, and increased reactive oxygen species (ROS) production. Functionally, SuHx-MVECs exhibited increased basal levels of intracellular calcium concentration ([Ca
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.