Evidence map›Paper›PMID 36370710›Full record

ArticleNeuron2023

Driving axon regeneration by orchestrating neuronal and non-neuronal innate immune responses via the IFNγ-cGAS-STING axis.

Xu Wang, Chao Yang, Xuejie Wang, Jinmin Miao, Weitao Chen, Yiren Zhou, Ying Xu, Yongyan An, Aifang Cheng, Wenkang Ye and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Neuron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.0field-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

50 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Expanding roles of cGAS-STING signaling in neuroinflammation.The Journal of clinical investigation · 2026
    Review
  7. Article
  8. Review
  9. Molecular Signatures of Id2- and Ascl4-Induced Wiring of Adult Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Amyloid-beta glycation induces neuronal mitochondrial dysfunction and Alzheimer's pathogenesis via VDAC1-dependent mtDNA efflux.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 2 institutions in 3 countries.

Xu WangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Biomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China; Guangdong Provincial Key Laboratory of Brain Science, Disease and Drug Development, HKUST Shenzhen Research Institute, Shenzhen-Hong Kong Institute of Brain Science, Shenzhen, Guangdong 518057, China; Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangzhou 510515, China.
Chao YangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Biomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China; Guangdong Provincial Key Laboratory of Brain Science, Disease and Drug Development, HKUST Shenzhen Research Institute, Shenzhen-Hong Kong Institute of Brain Science, Shenzhen, Guangdong 518057, China; Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangzhou 510515, China.
Xuejie WangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China.
Jinmin MiaoDepartment of Medicinal Chemistry and Molecular Pharmacology, Department of Chemistry, Center for Cancer Research and Institute for Drug Discovery, Purdue University, West Lafayette, IN, USA.
Weitao ChenBiomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China.
Yiren ZhouDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Ying XuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Department of Chemical and Biological Engineering, The Hong Kong University of Science and Technology, Hong Kong, China.
Yongyan AnDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Aifang ChengSouthern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Department of Ocean Science, The Hong Kong University of Science and Technology, Hong Kong, China.
Wenkang YeSouthern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Department of Ocean Science, The Hong Kong University of Science and Technology, Hong Kong, China.
Mengxian ChenDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Dong SongDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Department of Chemical and Biological Engineering, The Hong Kong University of Science and Technology, Hong Kong, China.
Xue YuanHong Kong Center for Neurodegenerative Diseases, Hong Kong, China.
Jiguang WangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Department of Chemical and Biological Engineering, The Hong Kong University of Science and Technology, Hong Kong, China.
Peiyuan QianSouthern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Department of Ocean Science, The Hong Kong University of Science and Technology, Hong Kong, China.
Angela Ruohao WuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Department of Chemical and Biological Engineering, The Hong Kong University of Science and Technology, Hong Kong, China; Center for Aging Science, The Hong Kong University of Science and Technology, Hong Kong, China.
Zhong-Yin ZhangDepartment of Medicinal Chemistry and Molecular Pharmacology, Department of Chemistry, Center for Cancer Research and Institute for Drug Discovery, Purdue University, West Lafayette, IN, USA.
Kai LiuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China; Southern Marine Science and Engineering Guangdong Laboratory (Guangzhou), Guangzhou, China; Biomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China; Guangdong Provincial Key Laboratory of Brain Science, Disease and Drug Development, HKUST Shenzhen Research Institute, Shenzhen-Hong Kong Institute of Brain Science, Shenzhen, Guangdong 518057, China; Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangzhou 510515, China. Electronic address: kailiu@ust.hk.
Hong Kong University of Science and Technology · HKPurdue University West Lafayette · US

Funding

Structure/Function of Protein Tyrosine PhosphatasesR01CA069202 · NCI · YESHIVA UNIVERSITY · PI Zhong-Yin Zhang · 1996 to 2026
$7.3M
NCI NIH HHS R01 CA069202
6 · The paper itself

Abstract

The coordination mechanism of neural innate immune responses for axon regeneration is not well understood. Here, we showed that neuronal deletion of protein tyrosine phosphatase non-receptor type 2 sustains the IFNγ-STAT1 activity in retinal ganglion cells (RGCs) to promote axon regeneration after injury, independent of mTOR or STAT3. DNA-damage-induced cGAMP synthase (cGAS)-stimulator of interferon genes (STINGs) activation is the functional downstream signaling. Directly activating neuronal STING by cGAMP promotes axon regeneration. In contrast to the central axons, IFNγ is locally translated in the injured peripheral axons and upregulates cGAS expression in Schwann cells and infiltrating blood cells to produce cGAMP, which promotes spontaneous axon regeneration as an immunotransmitter. Our study demonstrates that injured peripheral nervous system (PNS) axons can direct the environmental innate immune response for self-repair and that the neural antiviral mechanism can be harnessed to promote axon regeneration in the central nervous system (CNS).

Indexed as

AxonsNerve RegenerationImmunity, InnateNucleotidyltransferasesRetinal Ganglion CellsNucleotidyltransferasesaxon regenerationcGAS-STINGdorsal root ganglionsinterferon gammaoptic nerve injuryPTPN2retinal ganglion cellsSTAT1

Identifiers

PMID36370710
PMCPMC9851977
OpenAlexW4308806503

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.