Evidence map›Paper›PMID 39147737›Full record

ArticleCell death & disease2024

Toll-like receptor 4 deficiency in Purkinje neurons drives cerebellar ataxia by impairing the BK channel-mediated after-hyperpolarization and cytosolic calcium homeostasis.

Jianwei Zhu, Wenqiao Qiu, Fan Wei, Jin Zhang, Ying Yuan, Ling Liu, Meixiong Cheng, Huan Xiong, Ruxiang Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. 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

9 authors.

Jianwei Zhu *Department of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Wenqiao Qiu *Department of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Fan WeiDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Jin ZhangDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Ying YuanDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.ORCID 0009-0008-7407-7832
Ling LiuDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Meixiong ChengDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Huan XiongDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China. huan_xiong@163.com.
Ruxiang XuDepartment of Neurosurgery, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, China. xuruxiang1123@uestc.edu.cn.

Funding

China Postdoctoral Science Foundation 2021M700699Department of Science and Technology of Sichuan Province (Sichuan Provincial Department of Science and Technology) 2024NSFSC0614National Natural Science Foundation of China (National Science Foundation of China) 82001216National Natural Science Foundation of China (National Science Foundation of China) 82171355
6 · The paper itself

Abstract

Toll-like receptor (TLR) 4 contributes to be the induction of neuroinflammation by recognizing pathology-associated ligands and activating microglia. In addition, numerous physiological signaling factors act as agonists or antagonists of TLR4 expressed by non-immune cells. Recently, TLR4 was found to be highly expressed in cerebellar Purkinje neurons (PNs) and involved in the maintenance of motor coordination through non-immune pathways, but the precise mechanisms remain unclear. Here we report that mice with PN specific TLR4 deletion (TLR4

Indexed as

CalciumCerebellar AtaxiaLarge-Conductance Calcium-Activated Potassium ChannelsPurkinje CellsToll-Like Receptor 4AnimalsCytosolHomeostasisMiceMice, Inbred C57BLMice, KnockoutMitochondriaCalciumLarge-Conductance Calcium-Activated Potassium ChannelsTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID39147737
PMCPMC11327311

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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.