Evidence map›Paper›PMID 25023795›Full record

ArticleNature communications2014

H2S and NO cooperatively regulate vascular tone by activating a neuroendocrine HNO-TRPA1-CGRP signalling pathway.

Mirjam Eberhardt, Maria Dux, Barbara Namer, Jan Miljkovic, Nada Cordasic, Christine Will, Tatjana I Kichko, Jeanne de la Roche, Michael Fischer, Sebastián A Suárez and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers.

0numbers the graph read from it
0cells of the map it votes in
159citing papers in PubMed
17.4field-weighted citation impact, top 1% 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

159 citing papers in PubMed, 369 citations in OpenAlex.

  1. Trial
  2. A Human TRPA1-Specific Pain Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Trial
  3. Review
  4. Article
  5. Chemogenetic Manipulation of HPrecision chemistry · 2026
    Article
  6. Naturally Occurring HHandbook of experimental pharmacology · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Black gas, bright future: HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Review
  13. Hydrogen sulfide/polysulfides signaling and neuronal diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

99 more citing papers are in PubMed but not listed here.

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

25 authors at 9 institutions in 6 countries.

Mirjam Eberhardt1] Department of Chemistry and Pharmacy, Friedrich-Alexander University Erlangen-Nuremberg, Egerlandstrasse 1, 91058 Erlangen, Germany [2] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [3] Department of Anesthesiology and Intensive Care, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Maria Dux1] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [2] Department of Physiology, University of Szeged, Dóm tér 10, H-6720 Szeged, Hungary.
Barbara NamerInstitute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany.
Jan MiljkovicDepartment of Chemistry and Pharmacy, Friedrich-Alexander University Erlangen-Nuremberg, Egerlandstrasse 1, 91058 Erlangen, Germany.
Nada CordasicDepartment of Nephrology and Hypertension, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
Christine WillInstitute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany.
Tatjana I KichkoInstitute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany.
Jeanne de la RocheDepartment of Anesthesiology and Intensive Care, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Michael Fischer1] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [2] Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB1 2PD, UK.
Sebastián A SuárezDepartamento de Química Inorgánica, Analítica y Química Física/INQUIMAE-CONICET, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, C1428EHA, Buenos Aires, Argentina.
Damian BikielDepartamento de Química Inorgánica, Analítica y Química Física/INQUIMAE-CONICET, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, C1428EHA, Buenos Aires, Argentina.
Karola DorschInstitute of Pathology, University of Ulm, Albert-Einstein-Allee 23, 89070 Ulm, Germany.
Andreas LefflerDepartment of Anesthesiology and Intensive Care, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Alexandru Babes1] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [2] Department of Anatomy, Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independentei 91-95, 050095 Bucharest, Romania.
Angelika Lampert1] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [2].
Jochen K LennerzInstitute of Pathology, University of Ulm, Albert-Einstein-Allee 23, 89070 Ulm, Germany.
Johannes JacobiDepartment of Nephrology and Hypertension, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
Marcelo A Martí1] Departamento de Química Inorgánica, Analítica y Química Física/INQUIMAE-CONICET, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, C1428EHA, Buenos Aires, Argentina [2] Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, C1428EHA, Buenos Aires, Argentina.
Fabio DoctorovichDepartamento de Química Inorgánica, Analítica y Química Física/INQUIMAE-CONICET, Universidad de Buenos Aires, Ciudad Universitaria, Pab. II, C1428EHA, Buenos Aires, Argentina.
Edward D HögestättClinical Chemistry & Pharmacology, Department of Laboratory Medicine, Lund University Hospital, SE-221 85 Lund, Sweden.
Peter M ZygmuntClinical Chemistry & Pharmacology, Department of Laboratory Medicine, Lund University Hospital, SE-221 85 Lund, Sweden.
Ivana Ivanovic-BurmazovicDepartment of Chemistry and Pharmacy, Friedrich-Alexander University Erlangen-Nuremberg, Egerlandstrasse 1, 91058 Erlangen, Germany.
Karl MesslingerInstitute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany.
Peter Reeh1] Institute of Physiology and Pathophysiology Friedrich-Alexander University Erlangen-Nuremberg, Universitaetsstrasse 17, 91054 Erlangen, Germany [2].
Milos R Filipovic1] Department of Chemistry and Pharmacy, Friedrich-Alexander University Erlangen-Nuremberg, Egerlandstrasse 1, 91058 Erlangen, Germany [2].
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEConsejo Nacional de Investigaciones Científicas y Técnicas · ARLund University · SEMedizinische Hochschule Hannover · DEUniversität Ulm · DEFundación Ciencias Exactas y Naturales · ARRWTH Aachen University · DEUniversity of Buenos Aires · ARUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitroxyl (HNO) is a redox sibling of nitric oxide (NO) that targets distinct signalling pathways with pharmacological endpoints of high significance in the treatment of heart failure. Beneficial HNO effects depend, in part, on its ability to release calcitonin gene-related peptide (CGRP) through an unidentified mechanism. Here we propose that HNO is generated as a result of the reaction of the two gasotransmitters NO and H2S. We show that H2S and NO production colocalizes with transient receptor potential channel A1 (TRPA1), and that HNO activates the sensory chemoreceptor channel TRPA1 via formation of amino-terminal disulphide bonds, which results in sustained calcium influx. As a consequence, CGRP is released, which induces local and systemic vasodilation. H2S-evoked vasodilatatory effects largely depend on NO production and activation of HNO-TRPA1-CGRP pathway. We propose that this neuroendocrine HNO-TRPA1-CGRP signalling pathway constitutes an essential element for the control of vascular tone throughout the cardiovascular system.

Indexed as

AnimalsAortaBrain StemCalcitonin Gene-Related PeptideHumansHydrogen SulfideImmunohistochemistryIn Vitro TechniquesMiceMice, KnockoutNitric OxideNitrogen OxidesSignal TransductionSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationTransient Receptor Potential ChannelsTrigeminal GanglionCalcitonin Gene-Related PeptideHydrogen SulfideNitric OxideNitrogen OxidesnitroxylTransient Receptor Potential ChannelsTRPA1 Cation ChannelTrpa1 protein, mouse

Identifiers

PMID25023795
PMCPMC4104458
OpenAlexW2073091344

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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.