Evidence map›Paper›PMID 38639443›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Apoptotic Bodies Derived from Fibroblast-Like Cells in Subcutaneous Connective Tissue Inhibit Ferroptosis in Ischaemic Flaps via the miR-339-5p/KEAP1/Nrf2 Axis.

Gaoxiang Yu, Yijie Chen, Ningning Yang, Haojie Zhang, Xuzi Zhang, Yibo Geng, Jiayi Zhao, Zhuliu Chen, Chengji Dong, Lidan Lin and 9 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

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  19. Gut microbes · 2025
    Article
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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

19 authors.

Gaoxiang YuDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Yijie ChenDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
Ningning YangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Haojie ZhangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Xuzi ZhangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Yibo GengDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Jiayi ZhaoThe Second Clinical Medical College of Wenzhou Medical University, Wenzhou, 325027, China.
Zhuliu ChenDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Chengji DongDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Lidan LinZhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, 325027, China.
Jianjun QiDepartment of Clinical Laboratory, The First Affiliated Hospital of Wannan Medical College, Wuhu, Anhui, 241001, China.
Xuanlong ZhangZhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, 325027, China.
Xiaoqiong JiangZhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, 325027, China.
Weiyang GaoDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Yuepiao CaiMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325000, China.
Xiangyang WangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Jian DingDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.
Jian XiaoMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325000, China.
Kailiang ZhouDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.ORCID 0000-0001-7795-576X

Funding

Educational Commission Foundation of Anhui Province 2023AH040262Key Project of Wannan Medical College WK2022ZF20National Natural Science Foundation of China 82072192National Natural Science Foundation of China 82372540Project of Anhui Provincial Health Commission AHWJ2022b054Talent Research Fund Program of the First Hospital Affiliated to Wannan Medical College YR20220215Zhejiang Provincial Medical and Health Technology Plan Project 2024KY155Zhejiang Provincial Natural Science Foundation LY24H110002
6 · The paper itself

Abstract

Preventing and treating avascular necrosis at the distal end of the flaps are critical to surgery success, but current treatments are not ideal. A recent study shows that apoptotic bodies (ABs) generated near the site of apoptosis can be taken up and promote cell proliferation. The study reveals that ABs derived from fibroblast-like cells in the subcutaneous connective tissue (FSCT cells) of skin flaps promoted ischaemic flap survival. It is also found that ABs inhibited cell death and oxidative stress and promoted M1-to-M2 polarization in macrophages. Transcriptome sequencing and protein level testing demonstrated that ABs promoted ischaemic flap survival in endothelial cells and macrophages by inhibiting ferroptosis via the KEAP1-Nrf2 axis. Furthermore, microRNA (miR) sequencing data and in vitro and in vivo experiments demonstrated that ABs inhibited KEAP1 by delivering miR-339-5p to exert therapeutic effects. In conclusion, FSCT cell-derived ABs inhibited ferroptosis, promoted the macrophage M1-to-M2 transition via the miR-339-5p/KEAP1/Nrf2 axis and promoted ischaemic flap survival. These results provide a potential therapeutic strategy to promote ischaemic flap survival by administering ABs.

Indexed as

FerroptosisFibroblastsKelch-Like ECH-Associated Protein 1MicroRNAsNF-E2-Related Factor 2Surgical FlapsAnimalsApoptosisConnective TissueDisease Models, AnimalIschemiaMaleMiceSignal TransductionKeap1 protein, mouseKelch-Like ECH-Associated Protein 1MicroRNAsNF-E2-Related Factor 2apoptotic bodiesferroptosisischaemic flapsKEAP1‐Nrf2miR‐339‐5p

Identifiers

PMID38639443
PMCPMC11200024

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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.