Evidence map›Paper›PMID 24684551›Full record

ReviewAntioxidants & redox signaling2015

Modes of physiologic H2S signaling in the brain and peripheral tissues.

Bindu D Paul, Solomon H Snyder

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Intersection of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  4. Article
  5. Article
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  9. Review
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  11. Review
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  13. Article
  14. Review
  15. Inhalative as well as Intravenous Administration of HInternational journal of molecular sciences · 2022
    Article
  16. Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Bindu D Paul1 The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine , Baltimore, Maryland.
Solomon H Snyder
Johns Hopkins University · US

Funding

UNDERSTANDING NO SIGNALING RESULTING IN NEUROPROTECTION.P50DA000266 · NIDA · JOHNS HOPKINS UNIVERSITY · PI WORLEY, PAUL F · 1985 to 2017
$45.2M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR37MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1990 to 2009
$11.5M
NEUROCHEMICAL ACTIONS OF PSYCHOTROPIC DRUGSR01MH018501 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SNYDER, SOLOMON H. · 1985 to 2019
$10.8M
NIDA NIH HHS DA 000266NIMH NIH HHS MH18501
6 · The paper itself

Abstract

significanceHydrogen sulfide (H2S), once associated with rotten eggs and sewers, is now recognized as a gasotransmitter that is synthesized in vivo in a regulated fashion. This ancient gaseous molecule has been retained throughout evolution to perform various roles in different life forms. H2S modulates important signaling functions in diverse cellular processes ranging from regulation of blood pressure to redox homeostasis. RECENT ADVANCES: One of the modes by which H2S signals is by post-translational modification of reactive cysteine residues in a process designated as sulfhydration, resulting in conversion of the -SH groups of target cysteine residues to -SSH. Using the modified biotin-switch assay and a fluorescent maleimide-based analysis, sulfhydration of several proteins has been detected in various cell types. Aberrant sulfhydration patterns occur in neurodegenerative conditions such as Parkinson's disease. CRITICAL ISSUES: The exact concentration, source of H2S, and conditions under which various stores of H2S are utilized have not been fully elucidated. Currently, available inhibitors of the biosynthetic enzymes of H2S lack sufficient specificity to shed light on detailed mechanisms of H2S action. Probes with a higher sensitivity that can reliably detect cellular and tissue H2S levels are yet to be developed. FUTURE DIRECTIONS: Availability of advanced probes and biosynthesis inhibitors would help in the measurement of real-time changes of endogenous H2S levels in an in vivo context. The study of the dynamics of sulfhydration and nitrosylation of critical cysteine residues of regulatory proteins involved in physiology and pathophysiology is an area of interest for the future.

Indexed as

Signal TransductionAnimalsBrainCardiovascular SystemGasotransmittersGastrointestinal TractHomeostasisHumansHydrogen SulfideInflammationMitochondriaNitric OxideOxidation-ReductionParkinson DiseaseProtein Processing, Post-TranslationalGasotransmittersHydrogen SulfideNitric Oxide

Identifiers

PMID24684551
PMCPMC4307159
OpenAlexW2079313641

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.