ReviewRespiratory physiology & neurobiology2010
Hypoxia-induced changes in pulmonary and systemic vascular resistance: where is the O2 sensor?
Review in Respiratory physiology & neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 76 citations in OpenAlex.
- Fenestration Re-creation for Early Fontan Deterioration: Long-Term Hemodynamic and Clinical Outcomes.Pediatric cardiology · 2026Article
- Unique Systemic Vasodilatation of Post-fontan Physiology Compared with Biventricular Physiology: How Different is it on the CI-SVRI Plot?Pediatric cardiology · 2026Article
- Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.Antioxidants (Basel, Switzerland) · 2025Review
- Fontan Circulation and High Cardiac Output State: A Forgotten Phenotype.CJC pediatric and congenital heart disease · 2025Article
- mTOR in the Development of Hypoxic Pulmonary Hypertension Associated with Cardiometabolic Risk Factors.International journal of molecular sciences · 2024Review
- Sequestosome 1 (p62) mitigates hypoxia-induced cardiac dysfunction by stabilizing hypoxia-inducible factor 1α and nuclear factor erythroid 2-related factor 2.Cardiovascular research · 2024Article
- The Role of Mitochondrial Dysfunction in Idiopathic Pulmonary Fibrosis: New Perspectives for a Challenging Disease.Biology · 2023Review
- Study Hypoxic Response under Cyclic Oxygen Gradients Generated in Microfluidic Devices Using Real-Time Fluorescence Imaging.Biosensors · 2022Article
- Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension.Journal of clinical medicine · 2022Review
- Hypoxic vasodilatory defect and pulmonary hypertension in mice lacking hemoglobin β-cysteine93 S-nitrosylation.JCI insight · 2022Article
- Dysregulation of the Nitric Oxide/Dimethylarginine Pathway in Hypoxic Pulmonary Vasoconstriction-Molecular Mechanisms and Clinical Significance.Frontiers in medicine · 2022Review
- Regulation of Oxygen Homeostasis at the Intestinal Epithelial Barrier Site.International journal of molecular sciences · 2021Review
- Systemic Artery Vasoconstrictor Therapy in Fontan Patients with High Cardiac Output-Heart Failure: A Single-Center Experience.Pediatric cardiology · 2021Article
- Pulmonary Hypertension in Acute and Chronic High Altitude Maladaptation Disorders.International journal of environmental research and public health · 2021Review
- Embryo and Its Mitochondria.Antioxidants (Basel, Switzerland) · 2021Review
- AMPK and Pulmonary Hypertension: Crossroads Between Vasoconstriction and Vascular Remodeling.Frontiers in cell and developmental biology · 2021Review
- Redox Signaling and Regional Heterogeneity of Endothelial Dysfunction inInternational journal of molecular sciences · 2020Article
- Long Range Endocrine Delivery of Circulating miR-210 to Endothelium Promotes Pulmonary Hypertension.Circulation research · 2020Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Where Is the "Optimal" Fontan Hemodynamics?Korean circulation journal · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Pulmonary arteries (PA) constrict in response to alveolar hypoxia, whereas systemic arteries (SA) undergo dilation. These physiological responses reflect the need to improve gas exchange in the lung, and to enhance the delivery of blood to hypoxic systemic tissues. An important unresolved question relates to the underlying mechanism by which the vascular cells detect a decrease in oxygen tension and translate that into a signal that triggers the functional response. A growing body of work implicates the mitochondria, which appear to function as O2 sensors by initiating a redox-signaling pathway that leads to the activation of downstream effectors that regulate vascular tone. However, the direction of this redox signal has been the subject of controversy. Part of the problem has been the lack of appropriate tools to assess redox signaling in live cells. Recent advancements in the development of redox sensors have led to studies that help to clarify the nature of the hypoxia-induced redox signaling by reactive oxygen species (ROS). Moreover, these studies provide valuable insight regarding the basis for discrepancies in earlier studies of the hypoxia-induced mechanism of redox signaling. Based on recent work, it appears that the O2 sensing mechanism in both the PA and SA are identical, that mitochondria function as the site of O2 sensing, and that increased ROS release from these organelles leads to the activation of cell-specific, downstream vascular responses.
Indexed as
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.