Evidence map›Paper›PMID 24614199›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2014

Curcumin eliminates the effect of advanced glycation end-products (AGEs) on the divergent regulation of gene expression of receptors of AGEs by interrupting leptin signaling.

Youcai Tang, Anping Chen

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 68 citations in OpenAlex.

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  16. AGE-RAGE Axis in the Pathophysiology of Chronic Lower Limb Ischemia and a Novel Strategy for Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2020
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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

2 authors at 1 institution in 1 country.

Youcai TangDepartment of Pathology, School of Medicine, Saint Louis University, St Louis, MO, USA.
Anping ChenDepartment of Pathology, School of Medicine, Saint Louis University, St Louis, MO, USA.
Saint Louis University · US

Funding

REGULATION OF HEPATIC ITO CELL ACTIVATIONR01DK047995 · NIDDK · UNIVERSITY OF CHICAGO · PI CHEN, ANPING · 1995 to 2009
$2.1M
NIDDK NIH HHS R01 DK 047995NIDDK NIH HHS R01 DK047995
6 · The paper itself

Abstract

Non-alcoholic steatohepatitis (NASH) is a major risk factor for hepatic fibrogenesis. NASH is often found in diabetic patients with hyperglycemia. Hyperglycemia induces non-enzymatic glycation of proteins, yielding advanced glycation end-products (AGEs). Effects of AGEs are mainly mediated by two categories of cytoplasmic membrane receptors. Receptor for AGEs (RAGE) is associated with increased oxidative stress and inflammation, whereas AGE receptor-1 (AGE-R1) is involved in detoxification and clearance of AGEs. Activation of hepatic stellate cells (HSC) is crucial to the development of hepatic fibrosis. We recently reported that AGEs stimulated HSC activation likely by inhibiting gene expression of AGE-R1 and inducing gene expression of RAGE in HSC, which were eliminated by the antioxidant curcumin. This study is to test our hypothesis that curcumin eliminates the effects of AGEs on the divergent regulation of the two receptors of AGEs in HSC by interrupting the AGE-caused activation of leptin signaling, leading to the inhibition of HSC activation. We observed herein that AGEs activated leptin signaling by inducing gene expression of leptin and its receptor in HSC. Like AGEs, leptin differentially regulated gene expression of RAGE and AGE-R1. Curcumin eliminated the effects of AGEs in HSC by interrupting leptin signaling and activating transcription factor NF-E2 p45-related factor 2 (Nrf2), leading to the elevation of cellular glutathione and the attenuation of oxidative stress. In conclusions, curcumin eliminated the effects of AGEs on the divergent regulation of gene expression of RAGE and AGE-R1 in HSC by interrupting the AGE-caused activation of leptin signaling, leading to the inhibition of HSC activation.

Indexed as

AnimalsAntineoplastic AgentsCells, CulturedChromonesCurcumaCurcuminGene Expression RegulationGlycation End Products, AdvancedHepatic Stellate CellsLeptinLiver CirrhosisMaleMiceMice, Inbred C57BLMorpholinesPlant Extracts2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-onealpha-cyano-(3,4-dihydroxy)-N-benzylcinnamideAntineoplastic AgentsChromonesCurcuminGlycation End Products, AdvancedLeptinMorpholinesPlant ExtractsReceptor for Advanced Glycation End ProductsReceptors, ImmunologicReceptors, LeptinTyrphostins

Identifiers

PMID24614199
PMCPMC4006284
OpenAlexW2024854921

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.