Evidence map›Paper›PMID 24526678›Full record

ReviewCirculation research2014

Emergence of hydrogen sulfide as an endogenous gaseous signaling molecule in cardiovascular disease.

David J Polhemus, David J Lefer

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed
25.6field-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

199 citing papers in PubMed, 433 citations in OpenAlex.

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  6. The first and second zinc finger domains from Poly-ADP-ribose polymerase 1 (PARP1) are modified by hydrogen sulfide.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
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139 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

2 authors at 1 institution in 1 country.

David J PolhemusFrom the Department of Pharmacology, LSU Health Sciences Center, New Orleans, LA (D.J.P., D.J.L.); and the LSU Cardiovascular Center of Excellence, New Orleans, LA (D.J.P., D.J.L.).
David J Lefer
Louisiana State University Health Sciences Center New Orleans · US

Funding

Preclinical Consortium to Facilitate Translation of Cardioprotective TherapiesU24HL094373 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2010 to 2014
$9.6M
Functional Cardio-MetabolomicsP20HL113452 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L, TANG, WAI HONG WILSON · 2012 to 2016
$4.8M
Cardioprotective Actions of Hydrogen SulfideR01HL092141 · NHLBI · LSU HEALTH SCIENCES CENTER · PI LEFER, DAVID JOSEPH · 2009 to 2013
$1.9M
Nitrite Mediated CardioprotectionR01HL093579 · NHLBI · LSU HEALTH SCIENCES CENTER · PI LEFER, DAVID JOSEPH · 2009 to 2012
$1.5M
MECHANISMS OF MYOCARDIAL REPERFUSION INJURY IN DIABETESR01HL060849 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI LEFER, DAVID JOSEPH · 1999 to 2008
$1.5M
NHLBI NIH HHS 1P20 HL113452NHLBI NIH HHS 1R01 HL092141NHLBI NIH HHS 1R01 HL093579NHLBI NIH HHS 1U24 HL 094373NHLBI NIH HHS P20 HL113452NHLBI NIH HHS R01 HL060849NHLBI NIH HHS R01 HL092141NHLBI NIH HHS R01 HL093579NHLBI NIH HHS U24 HL094373
6 · The paper itself

Abstract

Long recognized as a malodorous and highly toxic gas, recent experimental studies have revealed that hydrogen sulfide (H2S) is produced enzymatically in all mammalian species including man and exerts several critical actions to promote cardiovascular homeostasis and health. During the past 15 years, scientists have determined that H2S is produced by 3 endogenous enzymes and exerts powerful effects on endothelial cells, smooth muscle cells, inflammatory cells, mitochondria, endoplasmic reticulum, and nuclear transcription factors. These effects have been reported in multiple organ systems, and the majority of data clearly indicate that H2S produced by the endogenous enzymes exerts cytoprotective actions. Recent preclinical studies investigating cardiovascular diseases have demonstrated that the administration of physiological or pharmacological levels of H2S attenuates myocardial injury, protects blood vessels, limits inflammation, and regulates blood pressure. H2S has emerged as a critical cardiovascular signaling molecule similar to nitric oxide and carbon monoxide with a profound effect on the heart and circulation. Our improved understanding of how H2S elicits protective actions, coupled with the rapid development of novel H2S-releasing agents, has resulted in heightened enthusiasm for the clinical translation of this ephemeral gaseous molecule. This review will examine our current state of knowledge about the actions of H2S within the cardiovascular system with an emphasis on the therapeutic potential and molecular cross talk between H2S, nitric oxide, and carbon monoxide.

Indexed as

AnimalsCarbon MonoxideCardiovascular DiseasesGasotransmittersHumansHydrogen SulfideNitric OxideSignal TransductionCarbon MonoxideGasotransmittersHydrogen SulfideNitric Oxidecarbon monoxidegasotransmittersheart failurenitric oxide

Identifiers

PMID24526678
PMCPMC3951140
OpenAlexW2120464741

What OpenQuestion holds

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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.