Evidence map›Paper›PMID 36157077›Full record

ReviewFrontiers in molecular neuroscience2022

Mitochondrial protein dysfunction in pathogenesis of neurological diseases.

Liang Wang, Ziyun Yang, Xiumei He, Shiming Pu, Cheng Yang, Qiong Wu, Zuping Zhou, Xiaobo Cen, Hongxia Zhao

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The First HeterozygousBiomolecules · 2025
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  11. Review
  12. Review
  13. Article
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  15. Article
  16. Review
  17. Review
  18. Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024
    Review
  19. Article
  20. Effects of carotenoids on mitochondrial dysfunction.Biochemical Society transactions · 2024
    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 at 3 institutions in 2 countries.

Liang WangNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Ziyun YangNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Xiumei HeSchool of Life Sciences, Guangxi Normal University, Guilin, China.
Shiming PuSchool of Life Sciences, Guangxi Normal University, Guilin, China.
Cheng YangSchool of Life Sciences, Guangxi Normal University, Guilin, China.
Qiong WuSchool of Life Sciences, Guangxi Normal University, Guilin, China.
Zuping ZhouGuangxi Universities, Key Laboratory of Stem Cell and Biopharmaceutical Technology, Guangxi Normal University, Guilin, China.
Xiaobo CenNational Chengdu Center for Safety Evaluation of Drugs, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Hongxia ZhaoSchool of Life Sciences, Guangxi Normal University, Guilin, China.
Guangxi Normal University · CNSichuan University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are essential organelles for neuronal function and cell survival. Besides the well-known bioenergetics, additional mitochondrial roles in calcium signaling, lipid biogenesis, regulation of reactive oxygen species, and apoptosis are pivotal in diverse cellular processes. The mitochondrial proteome encompasses about 1,500 proteins encoded by both the nuclear DNA and the maternally inherited mitochondrial DNA. Mutations in the nuclear or mitochondrial genome, or combinations of both, can result in mitochondrial protein deficiencies and mitochondrial malfunction. Therefore, mitochondrial quality control by proteins involved in various surveillance mechanisms is critical for neuronal integrity and viability. Abnormal proteins involved in mitochondrial bioenergetics, dynamics, mitophagy, import machinery, ion channels, and mitochondrial DNA maintenance have been linked to the pathogenesis of a number of neurological diseases. The goal of this review is to give an overview of these pathways and to summarize the interconnections between mitochondrial protein dysfunction and neurological diseases.

Indexed as

mitochondrial bioenergeticsmitochondrial dynamicsmitochondrial import machinerymitochondrial proteinsmitophagymtDNA maintenanceneurological diseasespathogenesis

Identifiers

PMID36157077
PMCPMC9489860
OpenAlexW4295024981

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.