ArticleInternational journal of molecular medicine2019
Melatonin restricts the viability and angiogenesis of vascular endothelial cells by suppressing HIF-1α/ROS/VEGF.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 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
104 citing papers in PubMed, 118 citations in OpenAlex.
- Sodium Sulfite as an Oxygen-Depletion-Based Chemical Model of Tumor Hypoxia In Vitro.Applied biochemistry and biotechnology · 2026Article
- Overexpression and knockdown of 5-lipoxygenase regulates the migration and invasion of colorectal cancer cells.Oncology letters · 2026Article
- Neuroprotective effects of agomelatine in a D-galactose-induced hippocampal aging model.Toxicology reports · 2026Article
- The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Evaluation of Local and Systemic Melatonin Administration on Bone Healing After Tooth Extraction in Bisphosphonate-Treated Rats.BMC oral health · 2026Article
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Natural bioactive compounds and herbal medicines targeting common signaling pathways in endometriosis: mechanisms and therapeutic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- A novel molecule ZYZ329 targeting histone methyltransferase SMYD3 suppresses pathological angiogenesis via the driven mitochondrial ROS/HIF-1α/VEGFA axis.Journal of translational medicine · 2026Article
- Selective recognition memory impairment in mitochondrial hydroxylase Clk1 mutant mice, rescued by antipsychotics.Acta pharmacologica Sinica · 2026Article
- Progress in the Cross-Organ Biomarker oxLDL in Promoting Pathological Neovascular Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Mechanisms of Luoshi Neiyi prescription (LSNYP) in endometriosis: a network pharmacology and experimental study.Hereditas · 2026Article
- Melatonin: A Silver Bullet for Fertility and Reproductive Health.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Hypoxia-induced regulations of cell adhesion molecules and their implications for pathogenesis, diagnosis, and treatment of endometriosis.Frontiers in molecular biosciences · 2026Review
- Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway.Biological trace element research · 2026Article
- ROS: their roles in diminished ovarian reserve.Frontiers in endocrinology · 2026Review
- Obesity and oxidative stress: potential mechanisms in endometrial disorders.Frontiers in endocrinology · 2026Review
- Inhibition of the HIF-1α Signaling Pathway Promotes Oligodendrocyte Maturation in the In Vitro Model of Perinatal Asphyxia.Molecular neurobiology · 2025Article
- A vascularized 3D bioengineered lung tumor model for anticancer drug screening.Cancer cell international · 2025Article
- SerpinB1a induces hepatopulmonary syndrome by promoting CTSG/AMPK/mTOR pathway-mediated mitophagy.Cell biology and toxicology · 2025Article
- Roles and Potential Mechanisms of Endothelial Cell-Derived Extracellular Vesicles in Ischemic Stroke.Translational stroke research · 2025Review
44 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 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenesis is an essential process involved in various physiological, including placentation, and pathological, including cancer and endometriosis, processes. Melatonin (MLT), a well‑known natural hormone secreted primarily in the pineal gland, is involved in regulating neoangiogenesis and inhibiting the development of a variety of cancer types, including lung and breast cancer. However, the specific mechanism of its anti‑angiogenesis activity has not been systematically elucidated. In the present study, the effect of MLT on viability and angiogenesis of human umbilical vein endothelial cells (HUVECs), and the production of vascular endothelial growth factor (VEGF) and reactive oxygen species (ROS), under normoxia or hypoxia was analyzed using Cell Counting kit 8, tube formation, flow cytometry, ELISA and western blot assays. It was determined that the secretion of VEGF by HUVECs was significantly increased under hypoxia, while MLT selectively obstructed VEGF release as well as the production of ROS under hypoxia. Furthermore, MLT inhibited the viability of HUVECs in a dose‑dependent manner and reversed the increase in cell viability and tube formation that was induced by hypoxia/VEGF/H2O2. Additionally, treatment with an inhibitor of hypoxia inducible factor (HIF)‑1α (KC7F2) and MLT synergistically reduced the release of ROS and VEGF, and inhibited cell viability and tube formation of HUVECs. These observations demonstrate that MLT may serve dual roles in the inhibition of angiogenesis, as an antioxidant and a free radical scavenging agent. MLT suppresses the viability and angiogenesis of HUVECs through the downregulation of HIF‑1α/ROS/VEGF. In summary, the present data indicate that MLT may be a potential anticancer agent in solid tumors with abundant blood vessels, particularly combined with KC7F2.
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.