Evidence map›Paper›PMID 29339732›Full record

ArticleScientific reports2018

Glyburide and retinoic acid synergize to promote wound healing by anti-inflammation and RIP140 degradation.

Yi-Wei Lin, Pu-Ste Liu, Kasey Ah Pook, Li-Na Wei

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

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-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

11 citing papers in PubMed, 29 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

4 authors at 1 institution in 1 country.

Yi-Wei LinDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, 55455, USA.
Pu-Ste LiuDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, 55455, USA.
Kasey Ah PookDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, 55455, USA.
Li-Na WeiDepartment of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota, 55455, USA. weixx009@umn.edu.
University of Minnesota Medical Center · US

Funding

Studies of nuclear receptor corepressor, NRIP1, in vitamin A signaling pathwaysR01DK060521 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 2002 to 2022
$6.9M
TR2 NUCLEAR RECEPTOR IN VITAMIN A SIGNALING PATHWAYSR01DK054733 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEI, LI-NA · 1999 to 2021
$5.7M
NIDDK NIH HHS R01 DK054733NIDDK NIH HHS R01 DK060521
6 · The paper itself

Abstract

Chronic inflammation underlies the development of metabolic diseases and individuals with metabolic disease often also suffer from delayed wound healing due to prolonged inflammation. Resolving inflammation provides a therapeutic strategy in treating metabolic diseases. We previously showed that during an anti-inflammatory response when macrophages were alternatively (M2) polarized, retinoic acid (RA) dramatically activated arginase 1 gene (Arg1), a gene crucial for wound healing. Here we report that a widely used sulfonylurea drug for type 2 diabetes mellitus (T2DM), glyburide, enhances the anti-inflammatory response and synergizes with RA to promote wound healing. Our data also delineate the mechanism underlying glyburide's anti-inflammatory effect, which is to stimulate the degradation of a pro-inflammatory regulator, Receptor Interacting Protein 140 (RIP140), by activating Ca2+/calmodulin-dependent protein kinase II (CamKII) that triggers specific ubiquitination of RIP140 for degradation. By stimulating RIP140 degradation, glyburide enhances M2 polarization and anti-inflammation. Using a high-fat diet induced obesity mouse model to monitor wound healing effects, we provide a proof-of-concept for a therapeutic strategy that combining glyburide and RA can significantly improve wound healing. Mechanistically, this study uncovers a new mechanism of action of glyburide and a new pathway modulating RIP140 protein degradation that is mediated by CamKII signaling.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedDiet, High-FatDrug SynergismGlyburideMacrophages, PeritonealMaleMiceMice, Inbred C57BLNuclear Receptor Co-Repressor 1ObesityPhosphorylationRAW 264.7 CellsSignal TransductionTretinoinCalcium-Calmodulin-Dependent Protein Kinase Type 2GlyburideNuclear Receptor Co-Repressor 1Tretinoin

Identifiers

PMID29339732
PMCPMC5770422
OpenAlexW2783476775

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.