ArticleAmerican journal of physiology. Cell physiology2017
ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.
Article in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 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.
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Who cites it
146 citing papers in PubMed, 240 citations in OpenAlex.
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- Metabolic reprogramming in diabetic panvascular disease: Molecular mechanism and therapeutic strategies.iScience · 2026Review
- An Update of Oxidative Stress in Atherosclerosis with Emphasis on the LOX-1-NLRP3 Inflammasome Axis.Current atherosclerosis reports · 2026Review
- Endothelial Drp1 integrates VEGF-induced redox signaling with glycolysis through cysteine oxidation to drive angiogenesis.Nature communications · 2026Article
- EndMT in vascular cognitive impairment and dementia: mechanisms, evidence gaps, and therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- Shikonin alleviates high-fat diet-induced vascular aging and dysfunction by inhibiting oxidative stress and mitochondrial damage.Molecular biology reports · 2026Article
- Dynamic regulation of receptor-modulated endothelial NADPH oxidases.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Catalase inhibits tumor growth by alleviating oxidative stress and promoting the polarization of tumor-associated macrophage from M2 to M1 phenotype in non-small cell lung cancer.Biology direct · 2026Article
- Microcirculatory failure after successful recanalization in ischemic stroke: insights into mechanisms, imaging, and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- BMP-Dependent Modulation of ROS Generation and Scavenging Controls Interdigital Cell Death.Development, growth & differentiation · 2026Article
- Oxidative Stress in DNA Damage and Neurodegenerative Diseases: Unveiling The Mechanisms and Therapeutic Opportunities.Cell biochemistry and biophysics · 2025Review
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Hypoxia preconditioned MSC exosomes attenuate high-altitude cerebral edema via the miR-125a-5p/RTEF-1 axis to protect vascular endothelial cells.Bioactive materials · 2025Article
- Active Endothelial Inactivation of Hyperpermeability: The Role of Nitric Oxide-Driven cAMP/Epac1 Signaling.Journal of cardiovascular development and disease · 2025Review
- Photodynamically tunable ROS-generating hydrogels for accelerated tissue regeneration.Bioactive materials · 2025Article
- Grazing-Induced Changes in circRNAs, miRNAs and mRNAs Expression in Tibetan Sheep Biceps Femoris.Biology · 2025Article
- The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025Review
- Reactive Oxygen Species: A Double-Edged Sword in the Modulation of Cancer Signaling Pathway Dynamics.Cells · 2025Review
86 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
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) and mitochondria play a critical role in growth factor-induced switch from a quiescent to an angiogenic phenotype in endothelial cells (ECs). However, how highly diffusible ROS produced from different sources can coordinate to stimulate VEGF signaling and drive the angiogenic process remains unknown. Using the cytosol- and mitochondria-targeted redox-sensitive RoGFP biosensors with real-time imaging, here we show that VEGF stimulation in human ECs rapidly increases cytosolic RoGFP oxidation within 1 min, followed by mitochondrial RoGFP oxidation within 5 min, which continues at least for 60 min. Silencing of Nox4 or Nox2 or overexpression of mitochondria-targeted catalase significantly inhibits VEGF-induced tyrosine phosphorylation of VEGF receptor type 2 (VEGFR2-pY), EC migration and proliferation at the similar extent. Exogenous hydrogen peroxide (H
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What Socratic 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 Socratic graph.