ReviewAntioxidants & redox signaling2010
ROS-dependent signaling mechanisms for hypoxic Ca(2+) responses in pulmonary artery myocytes.
Review in Antioxidants & redox signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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.
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- Differences in Milk Production Efficiency and Physiology Between Lactating Holstein Cows and Yaks Born and Kept at About 4000 m of Altitude When Fed the Same Diet.Journal of animal physiology and animal nutrition · 2025Article
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- Comparative DNA methylation reveals epigenetic adaptation to high altitude in snub-nosed monkeys.Zoological research · 2024Article
- Landscape genomics reveals regions associated with adaptive phenotypic and genetic variation in Ethiopian indigenous chickens.BMC genomics · 2024Article
- The "ON-OFF" Switching Response of Reactive Oxygen Species in Acute Normobaric Hypoxia: Preliminary Outcome.International journal of molecular sciences · 2023Article
- How Placenta Promotes the Successful Reproduction in High-Altitude Populations: A Transcriptome Comparison between Adaptation and Acclimatization.Molecular biology and evolution · 2022Article
- The Potential Important Role of Mitochondrial Rieske Iron-Sulfur Protein as a Novel Therapeutic Target for Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease.Biomedicines · 2022Review
- Important Functions and Molecular Mechanisms of Mitochondrial Redox Signaling in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2022Review
- Key miRNAs and Genes in the High-Altitude Adaptation of Tibetan Chickens.Frontiers in veterinary science · 2022Article
- Oxygen sensing, mitochondrial biology and experimental therapeutics for pulmonary hypertension and cancer.Free radical biology & medicine · 2021Article
- Endothelial cell-derived SSAO can increase MLCOpen life sciences · 2021Article
- Review - Nutraceuticals Can Target Asthmatic Bronchoconstriction: NADPH Oxidase-Dependent Oxidative Stress, RhoA and Calcium Dynamics.Journal of asthma and allergy · 2021Review
- Overview on Interactive Role of Inflammation, Reactive Oxygen Species, and Calcium Signaling in Asthma, COPD, and Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- Cellular and Molecular Processes in Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- Redox Signaling and Regional Heterogeneity of Endothelial Dysfunction inInternational journal of molecular sciences · 2020Article
- Rieske iron-sulfur protein induces FKBP12.6/RyR2 complex remodeling and subsequent pulmonary hypertension through NF-κB/cyclin D1 pathway.Nature communications · 2020Article
- Associations between geographical environment and systolic pulmonary arterial pressure of Chinese adults: impact analysis and predictive modeling.International journal of biometeorology · 2020Article
- Convergent genomic signatures of high-altitude adaptation among domestic mammals.National science review · 2020Article
- Important Role of Sarcoplasmic Reticulum CaAntioxidants & redox signaling · 2020Article
- PLCγ1-PKCε-IPAmerican journal of physiology. Lung cellular and molecular physiology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxic exposure causes pulmonary vasoconstriction, which serves as a critical physiologic process that ensures regional alveolar ventilation and pulmonary perfusion in the lungs, but may become an essential pathologic factor leading to pulmonary hypertension. Although the molecular mechanisms underlying hypoxic pulmonary vasoconstriction and associated pulmonary hypertension are uncertain, increasing evidence indicates that hypoxia can result in a significant increase in intracellular reactive oxygen species concentration ([ROS](i)) through the mitochondrial electron-transport chain in pulmonary artery smooth muscle cells (PASMCs). The increased mitochondrial ROS subsequently activate protein kinase C-epsilon (PKCepsilon) and NADPH oxidase (Nox), providing positive mechanisms that further increase [ROS](i). ROS may directly cause extracellular Ca(2+) influx by inhibiting voltage-dependent K(+) (K(V)) channels and opening of store-operated Ca(2+) (SOC) channels, as well as intracellular Ca(2+) release by activating ryanodine receptors (RyRs), leading to an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) and associated contraction. In concert with ROS, PKCepsilon may also affect K(V) channels, SOC channels, and RyRs, contributing to hypoxic Ca(2+) and contractile responses in PASMCs.
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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.