Evidence map›Paper›PMID 32627897›Full record

ArticleStem cells (Dayton, Ohio)2020

Allogeneic adipose-derived stem cells promote ischemic muscle repair by inducing M2 macrophage polarization via the HIF-1α/IL-10 pathway.

Junchao Liu, Peng Qiu, Jinbao Qin, Xiaoyu Wu, Xin Wang, Xinrui Yang, Bo Li, Wenjie Zhang, Kaichuang Ye, Zhiyou Peng and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 47 citations in OpenAlex.

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  15. MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024
    Review
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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

11 authors at 1 institution in 1 country.

Junchao LiuDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Peng QiuDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Jinbao QinDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Xiaoyu WuDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Xin WangDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Xinrui YangDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Bo LiDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Wenjie ZhangShanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Kaichuang YeDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Zhiyou PengDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.
Xinwu LuDepartment of Vascular Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.ORCID 0000-0001-6503-5210
Shanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China 81700432National Natural Science Foundation of China 81701801National Natural Science Foundation of China 81701842National Natural Science Foundation of China 81870346National Natural Science Foundation of China 81900410National Natural Science Foundation of China 81971758Shanghai Jiao Tong University School of Medicine Doctoral Innovation Fund BXJ201935
6 · The paper itself

Abstract

Adipose-derived mesenchymal stem cells (ASCs) are multipotent stromal cells that possess considerable therapeutic potential for tissue remodeling. However, their protective mechanism in critical limb ischemia has not been fully defined. After the occlusion of blood vessels, hypoxia becomes a prominent feature of the ischemic limb. This study investigated the immunomodulatory effect of ASCs on ischemic muscle repair and explored the specific mechanism. We found that the ability of RAW264.7 cells to migrate was impaired in hypoxia, whereas coculturing with ASCs could enhance the migration capacity. In addition, under hypoxic conditions, the paracrine effect of ASCs was enhanced and ASCs could induce RAW264.7 macrophages toward the anti-inflammatory M2 phenotype. We further demonstrated that ASCs-derived interleukin 10 (IL-10), mediated by hypoxia inducible factor-1α (HIF-1α), played a crucial role in the induction of M2 macrophages by activating the signal transducer and activator of transcription 3 (STAT3)/Arginase (Arg-1) pathway. Our in vivo experiments revealed that transplanted ASCs exhibited an immunomodulatory effect by recruiting macrophages to ischemic muscle and increasing the density of M2 macrophages. The transplantation of ASCs into ischemic limbs induced increased blood flow reperfusion and limb salvage rate, whereas the depletion of tissue macrophages or transplanting HIF-1α-silenced ASCs inhibited the therapeutic effect. These findings elucidated the critical role of macrophages in ASCs-mediated ischemic muscle repair and proved that allogeneic ASCs could exert the protective effect by enhancing the recruitment of macrophages and inducing macrophages toward M2 phenotype through HIF-1α/IL-10 pathway.

Indexed as

Stem Cell TransplantationAdipogenesisAdipose TissueAnimalsCell HypoxiaCell MovementCell PolarityCell ProliferationCell SurvivalGene SilencingHindlimbHypoxia-Inducible Factor 1, alpha SubunitInterleukin-10IschemiaMacrophagesMiceHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInterleukin-10adipose stem cellsangiogenesiscell transplantationhypoxiaskeletal muscle

Identifiers

PMID32627897
PMCPMC7590195
OpenAlexW3040487511

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.