ArticleBritish journal of pharmacology2012
Hydrogen sulfide inhibits the translational expression of hypoxia-inducible factor-1α.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 72 citations in OpenAlex.
- Molecular crosstalk between gas transmitters and catecholamine biosynthesis pathways: a narrative review.Medical gas research · 2027Review
- Review
- Systemic sodium hydrosulfide (NaHS) administration mitigates reperfusion injury in an experimental model of ischemic priapism.World journal of urology · 2026Article
- Hydrogen sulfide increases intracellular oxygen and inhibits the HIF response.The Journal of biological chemistry · 2026Article
- Power and poison: The intersections of HThe Journal of biological chemistry · 2025Review
- Hydrogen sulfide inhibits recruitment of monocyte-derived tumor associated macrophages in glioblastoma by downregulating CXCL12.Redox biology · 2025Article
- Cystathionine gamma-lyase-mediated hypoxia inducible factor 1-alpha expression drives clear cell ovarian cancer progression.The Journal of pathology · 2025Article
- Hydrogen Sulfide (HInternational journal of molecular sciences · 2025Review
- Hydrogen sulfide alleviates high-salt-stimulated myocardial fibrosis through inhibiting hypoxia-inducible factor-1α.Frontiers in pharmacology · 2025Article
- Signaling Paradigms of HAntioxidants (Basel, Switzerland) · 2024Review
- Hydrogen Sulfide Modulation of Matrix Metalloproteinases and CD147/EMMPRIN: Mechanistic Pathways and Impact on Atherosclerosis Progression.Biomedicines · 2024Review
- Membrane-Bound Ferric Hemoglobin in Nucleated Erythrocytes of the Black Scorpionfish Scorpaena porcus, Linnaeus 1758.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2024Article
- Role of Hydrogen Sulfide and Hypoxia in Hepatic Angiogenesis of Portal Hypertension.Journal of clinical and translational hepatology · 2023Review
- Role of hydrogen sulphide in physiological and pathological angiogenesis.Cell proliferation · 2023Review
- MPST sulfurtransferase maintains mitochondrial protein import and cellular bioenergetics to attenuate obesity.The Journal of experimental medicine · 2022Article
- Hypoxia-inducible factor 1-alpha is a driving mechanism linking chronic obstructive pulmonary disease to lung cancer.Frontiers in oncology · 2022Review
- A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism.Antioxidants (Basel, Switzerland) · 2021Review
- The Antiviral Roles of Hydrogen Sulfide by Blocking the Interaction between SARS-CoV-2 and Its Potential Cell Surface Receptors.Oxidative medicine and cellular longevity · 2021Review
- Cystathione β-synthase regulates HIF-1α stability through persulfidation of PHD2.Science advances · 2020Article
- Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe accumulation of hypoxia-inducible factor-1α (HIF-1α) is under the influence of hydrogen sulfide (H(2) S), which regulates hypoxia responses. The regulation of HIF-1α accumulation by H(2) S has been shown, but the mechanisms for this effect are largely elusive and controversial. This study aimed at addressing the controversial mechanisms for and the functional importance of the interaction of H(2) S and HIF-1α protein. EXPERIMENTAL APPROACH: HIF-1α protein levels and HIF-1α transcriptional activity were detected by Western blotting and luciferase assay. The mechanisms for H(2) S-regulated HIF-1α protein levels were determined using short interfering RNA transfection, co-immunoprecipitation and 7-methyl-GTP sepharose 4B pull-down assay. Angiogenic activity was evaluated using tube formation assay in EA.hy926 cells. KEY
resultsThe accumulation of HIF-1α protein under hypoxia (1% O(2) ) or hypoxia-mimetic conditions was reversed by sodium hydrosulfide (NaHS). This effect of NaHS was not altered after blocking the ubiquitin-proteasomal pathway for HIF-1α degradation; however, blockade of protein translation with cycloheximide abolished the effect of NaHS on the half-life of HIF-1α protein. Knockdown of eukaryotic translation initiation factor 2α (eIF2α) suppressed the effect of NaHS on HIF-1α protein accumulation under hypoxia. NaHS inhibited the expression of VEGF under hypoxia. It also decreased in vitro capillary tube formation and cell proliferation of EA.hy926 cells under hypoxia, but stimulated the tube formation under normoxia. CONCLUSIONS AND IMPLICATIONS: H(2) S suppresses HIF-1α translation by enhancing eIF2α phosphorylation under hypoxia. The interaction of H(2) S and HIF-1α inhibits the angiogenic activity of vascular endothelial cells under hypoxia through the down-regulation of VEGF.
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.