Evidence map›Paper›PMID 39292743›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

Lipin1 depletion coordinates neuronal signaling pathways to promote motor and sensory axon regeneration after spinal cord injury.

Weitao Chen, Junqiang Wu, Chao Yang, Suying Li, Zhewei Liu, Yongyan An, Xuejie Wang, Jiaming Cao, Jiahui Xu, Yangyang Duan and 8 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

18 authors.

Weitao Chen *Biomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China.ORCID 0000-0003-3504-011X
Junqiang Wu *Division of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0002-9029-3016
Chao Yang *Division of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Suying LiState Key Laboratory of Chemical Biology and Drug Discovery, Research Institute for Future Food, Research Centre for Chinese Medicine Innovation, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong Special Administrative Region, China.
Zhewei LiuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0003-1802-8979
Yongyan AnDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0003-3374-2046
Xuejie WangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Jiaming CaoDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Jiahui XuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Yangyang DuanDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0002-0823-6574
Xue YuanHong Kong Center for Neurodegenerative Diseases, Hong Kong, China.ORCID 0000-0003-0515-1847
Xin ZhangDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0002-8820-5128
Yiren ZhouDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Jacque Pak Kan IpSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.ORCID 0000-0003-4545-8261
Amy K Y FuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.
Nancy Y IpDivision of Life Science, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0002-2763-8907
Zhongping YaoState Key Laboratory of Chemical Biology and Drug Discovery, Research Institute for Future Food, Research Centre for Chinese Medicine Innovation, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong Special Administrative Region, China.ORCID 0000-0003-3555-9632
Kai LiuBiomedical Research Institute, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen 518036, China.ORCID 0000-0001-9351-1640

Funding

GDSTC | Natural Science Foundation of Guangdong Province () 2021A1515010856Guangzhou Key Projects of Brain Science and Brain-Like Intelligence Technology 20200730009Hong Kong Center for Neurodegenerative Diseases InnoHK of Hong Kong SAR, Health and Medical Reasearch Fund 06173946Hong Kong Research Grant Council 14117221Hong Kong Research Grant Council 15304020 R5013-19 R4005-18 and C4002-20WFHong Kong Research Grant Council 24117220Hong Kong Research Grant Council AoE/M-604/16Hong Kong Research Grant Council AoE/M-604/16 C6034-21G T13-602/21 N 16102519Innovation and Technology Commission (ITC) ITCPD/17-9MOST | National Natural Science Foundation of China (NSFC) 82171384Nan Fung Life Sciences (NFLS) noShenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions 2019SHIBS0001
6 · The paper itself

Abstract

Adult central nervous system (CNS) neurons down-regulate growth programs after injury, leading to persistent regeneration failure. Coordinated lipids metabolism is required to synthesize membrane components during axon regeneration. However, lipids also function as cell signaling molecules. Whether lipid signaling contributes to axon regeneration remains unclear. In this study, we showed that lipin1 orchestrates mechanistic target of rapamycin (mTOR) and STAT3 signaling pathways to determine axon regeneration. We established an mTOR-lipin1-phosphatidic acid/lysophosphatidic acid-mTOR loop that acts as a positive feedback inhibitory signaling, contributing to the persistent suppression of CNS axon regeneration following injury. In addition, lipin1 knockdown (KD) enhances corticospinal tract (CST) sprouting after unilateral pyramidotomy and promotes CST regeneration following complete spinal cord injury (SCI). Furthermore, lipin1 KD enhances sensory axon regeneration after SCI. Overall, our research reveals that lipin1 functions as a central regulator to coordinate mTOR and STAT3 signaling pathways in the CNS neurons and highlights the potential of lipin1 as a promising therapeutic target for promoting the regeneration of motor and sensory axons after SCI.

Indexed as

AxonsMotor NeuronsNerve RegenerationPhosphatidate PhosphataseSignal TransductionSpinal Cord InjuriesSTAT3 Transcription FactorTOR Serine-Threonine KinasesAnimalsFemaleMicePhosphatidic AcidsPyramidal TractsSensory Receptor CellsLpin1 protein, mousemTOR protein, mousePhosphatidate PhosphatasePhosphatidic AcidsStat3 protein, mouseSTAT3 Transcription FactorTOR Serine-Threonine Kinasesaxon regenerationlipid metabolismlipid signalinglipin1spinal cord injury

Identifiers

PMID39292743
PMCPMC11441493

What Socratic 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 Socratic graph.