Evidence map›Paper›PMID 27805071›Full record

ArticleScientific reports2016

AGEs Induced Autophagy Impairs Cutaneous Wound Healing via Stimulating Macrophage Polarization to M1 in Diabetes.

Yuanyuan Guo, Cai Lin, Peng Xu, Shan Wu, Xiujun Fu, Weidong Xia, Min Yao

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

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

Yuanyuan GuoDepartment of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine; Shanghai Jiao Tong University School of Medicine, Shanghai, 201900, China.
Cai LinBurn and Wound center, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Peng XuDepartment of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine; Shanghai Jiao Tong University School of Medicine, Shanghai, 201900, China.
Shan WuDepartment of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine; Shanghai Jiao Tong University School of Medicine, Shanghai, 201900, China.
Xiujun FuDepartment of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine; Shanghai Jiao Tong University School of Medicine, Shanghai, 201900, China.
Weidong XiaBurn and Wound center, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Min YaoDepartment of Burns and Plastic Surgery, Shanghai Ninth People's Hospital, Institute of Traumatic Medicine; Shanghai Jiao Tong University School of Medicine, Shanghai, 201900, China.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CNFirst Affiliated Hospital of Wenzhou Medical University · CNHarvard University · USWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is essential in physiological and pathological processes, however, the role of autophagy in cutaneous wound healing and the underlying molecular mechanism remain elusive. We hypothesized that autophagy plays an important role in regulating wound healing. Here, we show that enhanced autophagy negatively impacts on normal cutaneous healing process and is related to chronic wounds as demonstrated by the increased LC3 in diabetic mice skin or patients' chronic wounds. In addition, inhibition of autophagy by 3-MA restores delayed healing in C57BL/6 or db/db mice, demonstrating that autophagy is involved in regulating wound healing. Furthermore, we identify that macrophage is a major cell type underwent autophagy in wounds and increased autophagy induces macrophages polarization into M1 with elevated CD11c population and gene expressions of proinflammatory cytokines. To explore the mechanism underlying autophagy-impaired wound healing, we tested the role of IRF8, a regulator of autophagy, in autophagy-modulated macrophages polarization. IRF8 activation is up-regulating autophagy and M1 polarization of macrophages after AGEs (advanced glycation endproducts) treatment, blocking the IRF8 with shIRF8 inhibits autophagic activity and M1 polarization. In summary, this study elucidates that AGEs induces autophagy and modulates macrophage polarization to M1 via IRF8 activation in impairment of cutaneous wound healing.

Indexed as

AdenineAnimalsAutophagosomesAutophagyCD11c AntigenCytokinesDiabetes Mellitus, ExperimentalGlycation End Products, AdvancedInterferon Regulatory Factor-8Interferon Regulatory FactorsMacrophagesMaleMiceMice, Inbred C57BLMice, ObeseMicroscopy, Electron3-methyladenineAdenineCD11c AntigenCytokinesGlycation End Products, AdvancedInterferon Regulatory Factor-8Interferon Regulatory FactorsRNA, Small InterferingSirolimus

Identifiers

PMID27805071
PMCPMC5090347
OpenAlexW2548789381

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.