ArticleJournal of molecular medicine (Berlin, Germany)2013
Mitochondrial UQCRB regulates VEGFR2 signaling in endothelial cells.
Article in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- UQCRB regulates mitochondrial energy metabolism by promoting COX5 A in atherosclerotic endothelial dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025Review
- UQCRB and LBH are correlated with Gleason score progression in prostate cancer: Spatial transcriptomics and experimental validation.Computational and structural biotechnology journal · 2024Article
- Metabolic Regulation of Endothelial Cells: A New Era for Treating Wet Age-Related Macular Degeneration.International journal of molecular sciences · 2024Review
- Mitochondria in endothelial cells angiogenesis and function: current understanding and future perspectives.Journal of translational medicine · 2023Review
- Targeting Mitochondrial ROS Production to Reverse the Epithelial-Mesenchymal Transition in Breast Cancer Cells.Current issues in molecular biology · 2022Article
- Mitochondrial ROS Produced in Human Colon Carcinoma Associated with Cell Survival via Autophagy.Cancers · 2022Article
- The loss of DHX15 impairs endothelial energy metabolism, lymphatic drainage and tumor metastasis in mice.Communications biology · 2021Article
- Essential role for paxillin tyrosine phosphorylation in LPS-induced mitochondrial fission, ROS generation and lung endothelial barrier loss.Scientific reports · 2021Article
- Exploring gene knockout strategies to identify potential drug targets using genome-scale metabolic models.Scientific reports · 2021Article
- Sensors and signals: the role of reactive oxygen species in hypoxic pulmonary vasoconstriction.The Journal of physiology · 2019Review
- The role of mitochondria in angiogenesis.Molecular biology reports · 2019Review
- Bipolenins K-N: New sesquiterpenoids from the fungal plant pathogenBeilstein journal of organic chemistry · 2019Article
- Proteomic Analysis of Mouse Brain Subjected to Spaceflight.International journal of molecular sciences · 2018Article
- Discovery of novel drug targets and their functions using phenotypic screening of natural products.Journal of industrial microbiology & biotechnology · 2016Review
- The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.Human genetics · 2014Review
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledVascular endothelial growth factor (VEGF) signal transduction is involved in tumor angiogenesis, and the inhibition of this pathway is considered to be a powerful strategy for cancer therapy. We previously showed that small molecules targeting the ubiquinol-cytochrome c reductase binding protein (UQCRB), a subunit of mitochondrial complex III, in tumor cells suppress hypoxia-induced tumor angiogenesis. However, the mechanism by which UQCRB functioned remained unknown. In the present study, we demonstrate in endothelial cells (ECs) that UQCRB enhances VEGF receptor type 2 (VEGFR2) signaling by increasing the levels of mitochondrial reactive oxygen species (ROS). By contrast, terpestacin, a UQCRB targeting small molecule, blocked mitochondrial ROS-mediated VEGFR2 signaling pathways in ECs, thereby suppressing VEGF-dependent angiogenesis in vitro and in vivo. Furthermore, treatment with both terpestacin and bevacizumab, a VEGF signaling inhibitor, resulted in additive inhibition of tumor-induced angiogenesis both in vitro and in vivo. These data demonstrate that mitochondrial UQCRB positively regulates VEGFR2 signaling in ECs and the UQCRB targeting agent could be applied in new therapeutic approaches for human cancer. KEY MESSAGE: Inhibiting angiogenesis has been a focus for anti-cancer strategies. Mitochondrial UQCRB enhances VEGFR2 signaling by increasing ROS in endothelial cells. UQCRB inhibitor blocks angiogenesis by suppressing mitochondrial ROS. Findings may provide a new therapeutic approach for human cancer.
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.