Evidence map›Paper›PMID 28747872›Full record

ArticleFrontiers in neuroscience2017

L-3-n-Butylphthalide Protects HSPB8 K141N Mutation-Induced Oxidative Stress by Modulating the Mitochondrial Apoptotic and Nrf2 Pathways.

Xiao-Dong Yang, Zhi-Dong Cen, Hai-Peng Cheng, Kai Shi, Jie Bai, Fei Xie, Hong-Wei Wu, Bei-Bei Li, Wei Luo

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Article
  4. Neurological Applications of Celery (Molecules (Basel, Switzerland) · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Long-Term DL-3-Frontiers in aging neuroscience · 2018
    Article
  15. 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

9 authors.

Xiao-Dong YangDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.
Zhi-Dong CenDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.
Hai-Peng ChengDepartment of Neurology, Northwestern University Feinberg School of MedicineChicago, IL, United States.
Kai ShiDepartment of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao UniversityQingdao, China.
Jie BaiDepartment of Neurology, Qingdao No.8 People's HospitalQingdao, China.
Fei XieDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.
Hong-Wei WuDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.
Bei-Bei LiDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.
Wei LuoDepartment of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Charcot-Marie-Tooth disease (CMT), also known as hereditary motor and sensory neuropathy, is the most common inherited peripheral nerve disorder. Missense mutations, such as K141N, in the small heat shock protein HSPB8 are known to cause distal hereditary motor neuropathy 2A (dHMN2A) or Charcot-Marie-Tooth neuropathy type 2L (CMT2L). However, of critical clinical significance, very few specific therapies for this disease exist. In the present study, we investigated the impact of mutant K141N HSPB8 on mitochondrial distribution and function in a cellular model of CMT2L. Our results indicate that K141N HSPB8 induced mitochondrial aggregation and caused increased oxidative stress injury. As an extraction from Chinese celery Apium graveolens Linn seeds, L-3-n-Butylphthalide (NBP), has been reported to exert many neuroprotective effects, we interrogated whether NBP could elicit a protective effect on the cell injury typically caused by HSPB8 K141N mutations. We found NBP could reverse the pathological processes induced by HSPB8 K141N mutation via an antioxidant effect, modulation of the Bax/Bcl-2 mitochondrial apoptotic and Nrf2 pathways. We propose a novel function of HSPB8, highlighting the consequence of the K141N pathogenic mutation. Furthermore, we suggest NBP may have promising therapeutic potential in the treatment of CMT2L.

Indexed as

Charcot-Marie-Tooth diseaseL-3-n-butylphthalidemitochondrial dysfunctionoxidative stresssmall heat shock protein HSPB8

Identifiers

PMID28747872
PMCPMC5506380

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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.