ArticleRedox biology2021
Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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
5 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Sulfur Dioxide Alleviates Organ Damage and Inflammatory Response in Cecal Ligation and Puncture-Induced Sepsis Rat.Molecular biotechnology · 2025Article
- Fluorescent small molecule donors.Chemical Society reviews · 2024Review
- Advances in the research of sulfur dioxide and pulmonary hypertension.Frontiers in pharmacology · 2023Review
- Rodents on a high-fat diet born to mothers with gestational diabetes exhibit sex-specific lipidomic changes in reproductive organs.Acta biochimica et biophysica Sinica · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to determine the communicational pattern of gaseous signaling molecules sulfur dioxide (SO APPROACH AND
resultsBlood pressure was monitored by the tail-cuff and implantable physiological signal telemetry in L-nitro-arginine methyl ester (l-NAME)-induced hypertensive mice, and structural alterations of mouse aortic vessels were detected by the elastic fiber staining method. l-NAME-treated mice showed decreased plasma NO levels, increased SO
conclusionEndothelium-derived NO inhibits AAT activity by nitrosylating AAT1 at the Cys192 site and reduces SO
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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.