Evidence map›Paper›PMID 18685092›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Nitric oxide promotes distant organ protection: evidence for an endocrine role of nitric oxide.

John W Elrod, John W Calvert, Susheel Gundewar, Nathan S Bryan, David J Lefer

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 135 citations in OpenAlex.

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  20. Nitric oxide enhancement strategies.Future science OA · 2015
    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

5 authors at 2 institutions in 1 country.

John W ElrodDepartments of Medicine and Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
John W Calvert
Susheel Gundewar
Nathan S Bryan
David J Lefer
Albert Einstein College of Medicine · USBrown Foundation · US

Funding

MECHANISMS OF MYOCARDIAL REPERFUSION INJURY IN DIABETESR01HL060849 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI LEFER, DAVID JOSEPH · 1999 to 2008
$1.5M
Mechanisms of Nitrite Mediated Hepatic Preconditioning: Role of the MitochondriaF32DK077380 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI CALVERT, JOHN WINTER · 2006 to 2008
$74k
NHLBI NIH HHS 2R01 HL-060849NHLBI NIH HHS R01 HL060849NIDDK NIH HHS F32 DK077380NIDDK NIH HHS F32DK077380
6 · The paper itself

Abstract

Endothelial NOS (eNOS)-derived NO has long been considered a paracrine signaling molecule only capable of affecting nearby cells because of its short half-life in blood and relatively limited diffusion distance in tissues. To date, no studies have demonstrated that endogenously generated NO possesses a clearly defined endocrine function. Therefore, we evaluated whether enzymatic generation of NO in the heart is capable of modulating remote physiological actions and cell signaling. Mice with cardiac-specific overexpression of the human eNOS gene (CS-eNOS-Tg) were used to address this hypothesis. Cardiac-specific eNOS overexpression resulted in significant increases in nitrite, nitrate, and nitrosothiols in the heart, plasma, and liver. To examine whether the increase in hepatic NO metabolites could modulate cytoprotection, we subjected CS-eNOS-Tg mice to hepatic ischemia-reperfusion (I/R) injury. CS-eNOS-Tg mice displayed a significant reduction in hepatic I/R injury (4.2-fold reduction in the aminotransferase and a 3.5-fold reduction in aspartate aminotransferase) compared with WT littermates. These findings demonstrate that endogenously derived NO is transported in the blood, metabolized in remote organs, and mediates cytoprotection in the setting of I/R injury. This study presents clear evidence for an endocrine role of NO generated endogenously from eNOS and provides additional evidence for the profound cytoprotective actions of NO in the setting of I/R injury.

Indexed as

AnimalsBiological TransportCytoprotectionLiverMiceMice, TransgenicMyocardiumNitratesNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesOrgan SpecificityParacrine CommunicationReperfusion InjuryNitratesNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesNos3 protein, mouse

Identifiers

PMID18685092
PMCPMC2516252
OpenAlexW2078820537

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.