Evidence map›Paper›PMID 22718360›Full record

ArticleJournal of cellular physiology2013

Retinoic acid protects cardiomyocytes from high glucose-induced apoptosis through inhibition of NF-κB signaling pathway.

Irina T Nizamutdinova, Rakeshwar S Guleria, Amar B Singh, Jonathan A Kendall, Kenneth M Baker, Jing Pan

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 49 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

6 authors at 2 institutions in 1 country.

Irina T NizamutdinovaDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A&M Health Science Center, Temple, Texas 76504, USA.
Rakeshwar S Guleria
Amar B Singh
Jonathan A Kendall
Kenneth M Baker
Jing Pan
Baylor Scott & White Health · USTexas A&M Health Science Center · US

Funding

Role of Retinoid Mediated Signaling in Diabetes and Cardiac RemodelingR01HL091902 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI BAKER, KENNETH MELVIN · 2009 to 2010
$793k
NHLBI NIH HHS 1R01 HL091902NHLBI NIH HHS R01 HL091902
6 · The paper itself

Abstract

We have previously shown that retinoic acid (RA) has protective effects on high glucose (HG)-induced cardiomyocyte apoptosis. To further elucidate the molecular mechanisms of RA effects, we determined the interaction between nuclear factor (NF)-κB and RA signaling. HG induced a sustained phosphorylation of IKK/IκBα and transcriptional activation of NF-κB in cardiomyocytes. Activated NF-κB signaling has an important role in HG-induced cardiomyocyte apoptosis and gene expression of interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, and monocyte chemoattractant protein-1 (MCP-1). All-trans RA (ATRA) and LGD1069, through activation of RAR/RXR-mediated signaling, inhibited the HG-mediated effects in cardiomyocytes. The inhibitory effect of RA on NF-κB activation was mediated through inhibition of IKK/IκBα phosphorylation. ATRA and LGD1069 treatment promoted protein phosphatase 2A (PP2A) activity, which was significantly suppressed by HG stimulation. The RA effects on IKK and IκBα were blocked by okadaic acid or silencing the expression of PP2Ac-subunit, indicating that the inhibitory effect of RA on NF-κB is regulated through activation of PP2A and subsequent dephosphorylation of IKK/IκBα. Moreover, ATRA and LGD1069 reversed the decreased PP2A activity and inhibited the activation of IKK/IκBα and gene expression of MCP-1, IL-6, and TNF-α in the hearts of Zucker diabetic fatty rats. In summary, our findings suggest that the suppressed activation of PP2A contributed to sustained activation of NF-κB in HG-stimulated cardiomyocytes; and that the protective effect of RA on hyperglycemia-induced cardiomyocyte apoptosis and inflammatory responses is partially regulated through activation of PP2A and suppression of NF-κB-mediated signaling and downstream targets.

Indexed as

CytoprotectionAnimalsApoptosisBexaroteneCytokinesGene Expression RegulationHyperglycemiaI-kappa B KinaseMaleMyocytes, CardiacNF-kappa BPhosphorylationProtein Phosphatase 2RatsRats, ZuckerSignal TransductionBexaroteneCytokinesI-kappa B KinaseNF-kappa BProtein Phosphatase 2TetrahydronaphthalenesTretinoin

Identifiers

PMID22718360
PMCPMC3470832
OpenAlexW2077560317

What OpenQuestion holds

Textmetadata
LicenceTDM
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.