Evidence map›Paper›PMID 18495130›Full record

ArticleAtherosclerosis2009

Candesartan inhibits Toll-like receptor expression and activity both in vitro and in vivo.

Mohan R Dasu, Andrea C Riosvelasco, Ishwarlal Jialal

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 94 citations in OpenAlex.

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  13. MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021
    Review
  14. Review
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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

3 authors at 1 institution in 1 country.

Mohan R DasuLaboratory for Atherosclerosis and Metabolic Research, University of California Davis Medical Center, Sacramento, CA 95817, United States.
Andrea C Riosvelasco
Ishwarlal Jialal
University of California Davis Medical Center · US

Funding

Cellular pathways of inflammation in type 1 diabetesR33DK069801 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DEVARAJ, SRIDEVI · 2007 to 2008
$1.3M
CLINICAL STUDIES IN NUTRITION AND METABOLISMK24AT000596 · NCCIH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI JIALAL, ISHWARLAL · 2000 to 2009
$1.3M
Cellular pathways of inflammation in type 1 diabetesR21DK069801 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI DEVARAJ, SRIDEVI · 2004 to 2005
$747k
NCCIH NIH HHS K24 AT000596NCCIH NIH HHS K24 AT 00596NIDDK NIH HHS DK69801NIDDK NIH HHS R21 DK069801NIDDK NIH HHS R33 DK069801
6 · The paper itself

Abstract

introductionToll-like receptors play an important role in the innate immune system and are found to be crucial in severe diseases like sepsis, atherosclerosis, and arthritis. TLR2 and TLR4 expression is upregulated in the inflammatory diseases. Angiotensin II in addition to stimulating vasoconstriction also induces an increase in ROS and a proinflammatory phenotype via AT(1)R. Angiotensin II type-1 receptor blocker (ARB), widely used as an antihypertensive drug, has been reported to also have anti-inflammatory effects. Thus, we investigated whether an ARB exerts anti-inflammatory effects via inhibiting TLR2 and TLR4 expression. METHODS AND

resultsMonocytes were isolated from healthy human volunteers and treated with the synthetic lipoprotein Pam3CSK4 or LPS in the absence or presence of candesartan. Pretreatment of human monocytes with candesartan significantly decreased Pam3CSK4 or LPS induced TLR2 and TLR4 expression of both mRNA and protein levels (P<0.05 vs. control) along with decrease in the activity of NF-kappaB and the expression of IL-1beta, IL-6, TNF-alpha, and MCP-1. Furthermore, candesartan treated mice show decreased TLR2 and TLR4 expression compared to vehicle control mice.

conclusionPam3CSK4 and LPS induced TLR2 and TLR4 expression at mRNA and protein levels are inhibited by candesartan both in vitro and in vivo. Thus, we define a novel pathway by which candesartan could induce anti-inflammatory effects.

Indexed as

AnimalsAntihypertensive AgentsAnti-Inflammatory AgentsBenzimidazolesBiphenyl CompoundsGene Expression RegulationHumansInflammationIn Vitro TechniquesLipopeptidesMaleMiceMice, Inbred C57BLMonocytesPhenotypeReactive Oxygen SpeciesAntihypertensive AgentsAnti-Inflammatory AgentsBenzimidazolesBiphenyl CompoundscandesartanLipopeptidesPam(3)CSK(4) peptideReactive Oxygen SpeciesTetrazolesToll-Like Receptors

Identifiers

PMID18495130
PMCPMC2676176
OpenAlexW2048587489

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.