Evidence map›Paper›PMID 37387572›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023

Autophagosomes Defeat Ferroptosis by Decreasing Generation and Increasing Discharge of Free Fe

Shengnan Cui, Xi Liu, Yong Liu, Wenzhi Hu, Kui Ma, Qilin Huang, Ziqiang Chu, Lige Tian, Sheng Meng, Jianlong Su and 4 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 52 citations in OpenAlex.

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  2. Integrated OAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

14 authors at 6 institutions in 1 country.

Shengnan CuiDepartment of Dermatology, China Academy of Chinese Medical Science, Xiyuan Hospital, Beijing, 100091, China.
Xi LiuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Yong LiuDepartment of Dermatology, Shaanxi Provincial Hospital of Chinese Medicine, Xi'an, 710003, China.
Wenzhi HuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Kui MaResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Qilin HuangDepartment of the 4th Medical Center of Chinese PLA General Hospital, Tianjin Medical University, No. 22, Qixiangtai Road, Heping District, Tianjin, 300070, China.
Ziqiang ChuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Lige TianDepartment of the 4th Medical Center of Chinese PLA General Hospital, Tianjin Medical University, No. 22, Qixiangtai Road, Heping District, Tianjin, 300070, China.
Sheng MengResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Jianlong SuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Wenhua ZhangResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Haihong LiDepartment of Wound Repair, Institute of Wound Repair and Regeneration Medicine, Southern University of Science and Technology Hospital, Southern University of Science and Technology School of Medicine, Shenzhen, 518055, China.
Xiaobing FuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.
Cuiping ZhangResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Division, The 4th Medical Center of Chinese PLA General Hospital, Beijing, 100048, China.ORCID 0000-0003-0320-6226
Chinese PLA General Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNTianjin Medical University General Hospital · CNShaanxi Provincial Hospital of Traditional Chinese Medicine · CNSouthern University of Science and Technology · CNXiyuan Hospital · CN

Funding

CAMS Innovation Fund for Medical Sciences 2019-I2M-5-059CAMS Innovation Fund for Medical Sciences CIFMSMilitary Medical Research Projects 145AKJ260015000XMilitary Medical Research Projects 2022-JCJQ-ZB-09600Military Medical Science and Technology Youth Training Program 21QNPY128National Key Research and Development Programs of China 2022YFA1104303National Nature Science Foundation of China 22205260National Nature Science Foundation of China 81830064National Nature Science Foundation of China 82172211National Nature Science Foundation of China 82172231National Nature Science Foundation of China 92268206
6 · The paper itself

Abstract

Ferroptosis plays an essential role in the development of diabetes and its complications, suggesting potential therapeutic strategies targeting ferroptosis. Secretory autophagosomes (SAPs) carrying cytoplasmic cargoes have been recognized as novel nano-warrior to defeat diseases. Here, it is hypothesized that SAPs derived from human umbilical vein endothelial cells (HUVECs) can restore the function of skin repair cells by inhibiting ferroptosis to promote diabetic wound healing. High glucose (HG)-caused ferroptosis in human dermal fibroblasts (HDFs) is observed in vitro, which results in impaired cellular function. SAPs successfully inhibit ferroptosis in HG-HDFs, thereby improving their proliferation and migration. Further research show that the inhibitory effect of SAPs on ferroptosis resulted from a decrease in endoplasmic reticulum (ER) stress-regulated generation of free ferrous ions (Fe

Indexed as

Diabetes MellitusFerroptosisAutophagosomesHumansHuman Umbilical Vein Endothelial CellsWound Healingautophagosomesdiabetic woundsendoplasmic reticulum stressexosomesferroptosis

Identifiers

PMID37387572
PMCPMC10477857
OpenAlexW4382632603

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.