Evidence map›Paper›PMID 39158788›Full record

ArticleMolecular neurobiology2025

Microglia Promote Lymphangiogenesis Around the Spinal Cord Through VEGF-C/VEGFR3-Dependent Autophagy and Polarization After Acute Spinal Cord Injury.

Yeyang Xian, Jie Liu, Mengxuan Dai, Wensheng Zhang, Minye He, Zhengnong Wei, Yutao Jiang, Shiyong Le, Zhuoang Lin, Shuai Tang and 5 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. [Research progress on vascular endothelial growth factor C in meningeal lymphatic vessel-mediated clearance of amyloid β-protein].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  3. Review
  4. Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025
    Review
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

15 authors.

Yeyang Xian *Tianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Jie Liu *Tianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Mengxuan DaiTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Wensheng ZhangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Minye HeTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Zhengnong WeiTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Yutao JiangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Shiyong LeTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Zhuoang LinTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Shuai TangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Yunfei ZhouTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Liming DongTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Jinzheng LiangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China.
Jie ZhangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China. kamizj891026@126.com.
Liang WangTianhe District, Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Zhongshandadao West 183, Guangzhou City, 510000, China. liang091@aliyun.com.

Funding

National Natural Science Foundation of China 82072433Natural Science Foundation of Guangdong Province 2214050002081Science and Technology Program of Guangzhou, China 202102020768
6 · The paper itself

Abstract

Reducing secondary injury is a key focus in the field of spinal cord injury (SCI). Recent studies have revealed the role of lymphangiogenesis in reducing secondary damage to central nerve. However, the mechanism of lymphangiogenesis is not yet clear. Macrophages have been shown to play an important role in peripheral tissue lymphangiogenesis. Microglia is believed to play a role similar to macrophages in the central nervous system (CNS); we hypothesized that there was a close relationship between microglia and central nerve system lymphangiogenesis. Herein, we used an in vivo model of SCI to explored the relationship between microglia and spinal cord lymphangiogenesis and further investigated the polarization of microglia and its role in promoting spinal cord lymphangiogenesis by a series of in vitro experiments. The current study elucidated for the first time the relationship between microglia and lymphangiogenesis around the spinal cord after SCI. Classical activated (M1) microglia can promote lymphangiogenesis by secreting VEGF-C which further increases polarization and secretion of lymphatic growth factor by activating VEGFR3. The VEGF-C/VEGFR3 pathway activation downregulates microglia autophagy, thereby regulating the microglia phenotype. These results indicate that M1 microglia promote lymphangiogenesis after SCI, and activated VEGF-C/VEGFR3 signaling promotes M1 microglia polarization by inhibiting autophagy, thereby facilitates lymphangiogenesis.

Indexed as

AutophagyCell PolarityLymphangiogenesisMicrogliaSpinal CordSpinal Cord InjuriesVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-3AnimalsFemaleRats, Sprague-DawleySignal TransductionVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Receptor-3AutophagyLymphangiogenesisMicrogliaSpinal cord injuryVEGF-C

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Registered trials

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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.