Evidence map›Paper›PMID 38041169›Full record

ArticleMolecular neurodegeneration2023

MLKL deficiency alleviates neuroinflammation and motor deficits in the α-synuclein transgenic mouse model of Parkinson's disease.

Lu Geng, Wenqing Gao, Hexige Saiyin, Yuanyuan Li, Yu Zeng, Zhifei Zhang, Xue Li, Zuolong Liu, Qiang Gao, Ping An and 13 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurodegeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Necroptosis in Down Syndrome.Cell death & disease · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Mixed Lineage Kinase Domain-Like Protein (MLKL): From Mechanisms to Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  19. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  20. Article
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

23 authors at 7 institutions in 1 country.

Lu Geng *State Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Wenqing Gao *State Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Hexige SaiyinState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Yuanyuan LiState Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Yu ZengInsitute of Immunology, School of Medicine, Shanghai Jiaotong University, Shanghai, 200025, China.
Zhifei ZhangState Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Xue LiInsitute of Immunology, School of Medicine, Shanghai Jiaotong University, Shanghai, 200025, China.
Zuolong LiuState Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Qiang GaoState Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China.
Ping AnState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Ning JiangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xiaofei YuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Xiangjun ChenDepartment of Neurology, Huashan Hospital and Institute of Neurology, Fudan University, Shanghai, 200040, China.
Suhua LiDivision of Natural Science, Duke Kunshan University, Jiangsu, 215316, China.
Lei ChenInsitute of Immunology, School of Medicine, Shanghai Jiaotong University, Shanghai, 200025, China.
Boxun LuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, 200438, China.
Aiqun LiLevi Regenerative Medicine Technologies, Zhuhai, 519085, China.
Guoyuan ChenState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Yidong ShenState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Haibing ZhangCAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, Shanghai, 200031, China.
Mei TianHuman Phenome Institute, Fudan University, Shanghai, 200438, China.
Zhuohua ZhangInstitute of Molecular Precision Medicine, Xiangya Hospital, Central South University, Changsha, 410078, Hunan, China. zhangzhuohua@sklmg.edu.cn.
Jixi LiState Key Laboratory of Genetic Engineering, Department of Neurology, Huashan Hospital and School of Life Sciences, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, Fudan University, Shanghai, 200438, China. lijixi@fudan.edu.cn.ORCID 0000-0003-3463-3175
Fudan University · CNShanghai Jiao Tong University · CNCentral South University · CNChinese Academy of Sciences · CNCenter for High Pressure Science & Technology Advanced Research · CNDuke Kunshan University · CNShanghai Institute of Nutrition and Health · CN

Funding

National Natural Science Foundation of China 82071782
6 · The paper itself

Abstract

Parkinson's disease (PD), one of the most devastating neurodegenerative brain disorders, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and deposits of α-synuclein aggregates. Currently, pharmacological interventions for PD remain inadequate. The cell necroptosis executor protein MLKL (Mixed-lineage kinase domain-like) is involved in various diseases, including inflammatory bowel disease and neurodegenerative diseases; however, its precise role in PD remains unclear. Here, we investigated the neuroprotective role of MLKL inhibition or ablation against primary neuronal cells and human iPSC-derived midbrain organoids induced by toxic α-Synuclein preformed fibrils (PFFs). Using a mouse model (Tg-Mlkl

Indexed as

Parkinson Diseasealpha-SynucleinAnimalsDisease Models, AnimalDopaminergic NeuronsHumansMiceMice, KnockoutMice, TransgenicNeuroinflammatory DiseasesProtein KinasesSubstantia Nigraalpha-SynucleinMLKL protein, humanMLKL protein, mouseProtein KinasesSNCA protein, humanSnca protein, mouseMLKLNeuroinflammationParkinson’s diseasescRNA-seqTg-Mlkl −/− mice

Identifiers

PMID38041169
PMCPMC10693130
OpenAlexW4389223354

What OpenQuestion 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 OpenQuestion graph.