Evidence map›Paper›PMID 18211830›Full record

ReviewFree radical biology & medicine2008

Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases.

Roman Ginnan, Benjamin J Guikema, Katharine E Halligan, Harold A Singer, David Jourd'heuil

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-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

28 citing papers in PubMed, 63 citations in OpenAlex.

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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 1 institution in 1 country.

Roman GinnanCenter for Cardiovascular Sciences, Albany Medical College, Albany, NY 12208, USA.
Benjamin J Guikema
Katharine E Halligan
Harold A Singer
David Jourd'heuil
Albany Medical Center Hospital · US

Funding

CALCIUM/CALMODULIN ACTIVATED KINIASES IN SMOOTH MUSCLER01HL049426 · NHLBI · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI SINGER, HAROLD A · 1994 to 2019
$6.2M
TISSUE REMODELING AND CARDIOVASCULAR DISEASET32HL007194 · NHLBI · ALBANY MEDICAL COLLEGE · PI MC KEOWN-LONGO, PAULA J · 1985 to 2006
$2.9M
Mechanisms of Nitric Oxide Mediated Cell InjuryR01CA089366 · NCI · ALBANY MEDICAL COLLEGE · PI JOURD'HEUIL, DAVID · 2001 to 2005
$1.1M
PROTEIN KINASE C ACTIVATION IN ARTERIAL SMOOTH MUSCLER01HL040992 · NHLBI · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI SINGER, HAROLD A · 1988 to 2000
$193k
NCI NIH HHS CA-89366NCI NIH HHS R01 CA089366NHLBI NIH HHS R01 HL040992NHLBI NIH HHS R01 HL049426NHLBI NIH HHS R01-HL-40992NHLBI NIH HHS R01-HL-49426NHLBI NIH HHS T32 HL007194NHLBI NIH HHS T-32-HL-07194
6 · The paper itself

Abstract

Inflammation plays a critical role in promoting smooth muscle migration and proliferation during vascular diseases such as postangioplasty restenosis and atherosclerosis. Another common feature of many vascular diseases is the contribution of reactive oxygen (ROS) and reactive nitrogen (RNS) species to vascular injury. Primary sources of ROS and RNS in smooth muscle are several isoforms of NADPH oxidase (Nox) and the cytokine-regulated inducible nitric oxide (NO) synthase (iNOS). One important example of the interaction between NO and ROS is the reaction of NO with superoxide to yield peroxynitrite, which may contribute to the pathogenesis of hypertension. In this review, we discuss the literature that supports an alternate possibility: Nox-derived ROS modulate NO bioavailability by altering the expression of iNOS. We highlight data showing coexpression of iNOS and Nox in vascular smooth muscle demonstrating the functional consequences of iNOS and Nox during vascular injury. We describe the relevant literature demonstrating that the mitogen-activated protein kinases are important modulators of proinflammatory cytokine-dependent expression of iNOS. A central hypothesis discussed is that ROS-dependent regulation of the serine/threonine kinase protein kinase Cdelta is essential to understanding how Nox may regulate signaling pathways leading to iNOS expression. Overall, the integration of nonphagocytic NADPH oxidase with cytokine signaling in general and in vascular smooth muscle in particular is poorly understood and merits further investigation.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsCell ProliferationFree RadicalsHumansMAP Kinase Signaling SystemModels, BiologicalMyocytes, Smooth MuscleNADPH OxidasesNitric Oxide Synthase Type IIPhagocytosisProtein IsoformsProtein Kinase CReactive Oxygen SpeciesVascular DiseasesFree RadicalsNADPH OxidasesNitric Oxide Synthase Type IIProtein IsoformsProtein Kinase CReactive Oxygen Species

Identifiers

PMID18211830
PMCPMC2390910
OpenAlexW2089293555

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.