Evidence map›Paper›PMID 37082676›Full record

ReviewAnnals of translational medicine2023

Mitochondrial dynamics in neurological diseases: a narrative review.

Yue Shen, Wen-Li Jiang, Xin Li, Ai-Lin Cao, Dan Li, Shang-Ze Li, Jun Yang, Jiao Qian

Open access · diamondAbstract readReview
In one paragraph

Review in Annals of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Energy-dependent modulation of nucleus accumbens output via K-ATP channel activity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Article
  4. [DOT1L controls neuronal amyloid precursor protein expres-sion via the p38 MAPK-mediated mitochondrial dynamics homeostasis axis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Article
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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

8 authors at 4 institutions in 1 country.

Yue Shen *Department of Pharmacy, The First Affiliated Hospital (Changhai Hospital), Naval Medical University, Shanghai, China.
Wen-Li Jiang *Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Naval Medical University, Shanghai, China.
Xin Li *Department of Pharmacy, The First Affiliated Hospital (Changhai Hospital), Naval Medical University, Shanghai, China.
Ai-Lin CaoDepartment of Pharmacy, No. 905 Hospital of Navy, Shanghai, China.
Dan LiDepartment of Pharmacy, The First Affiliated Hospital (Changhai Hospital), Naval Medical University, Shanghai, China.
Shang-Ze LiDepartment of Orthopedics, The Second Affiliated Hospital (Changzheng Hospital), Naval Medical University, Shanghai, China.
Jun YangDepartment of Orthopedics, The Second Affiliated Hospital (Changzheng Hospital), Naval Medical University, Shanghai, China.
Jiao QianDepartment of Pharmacy, The First Affiliated Hospital (Changhai Hospital), Naval Medical University, Shanghai, China.
Changhai Hospital · CNShanghai Changzheng Hospital · CNPLA Navy General Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and Objective: The mitochondrion is a crucial organelle for aerobic respiration and energy metabolism. It undergoes dynamic changes, including changes in its shape, function, and distribution through fission, fusion, and movement. Under normal conditions, mitochondrial dynamics are in homeostasis. However, once the balance is upset, the nervous system, which has high metabolic demands, will most likely be affected. Recent studies have shown that the imbalance of mitochondrial dynamics is involved in the occurrence and development of various neurological diseases. However, whether the regulation of mitochondrial dynamics can be used to treat neurological diseases is still unclear. We aimed to comprehensively analyze mitochondrial dynamics regulation and its potential role in the treatment of neurological diseases. Methods: A comprehensive literature review was carried out to understand the mechanisms and applications of mitochondrial dynamics in neurological diseases based on the literature available in PubMed, Web of Science, and Google Scholar. Key Content and Findings: This review discusses the molecular mechanisms related to mitochondrial dynamics and expounds upon the role of mitochondrial dynamics in the occurrence and development of neurodegenerative diseases, epilepsy, cerebrovascular disease, and brain tumors. Several clinically tested drugs with fewer side effects have been shown to improve the mitochondrial dynamics and nervous system function in neurological diseases. Conclusions: Disorders of mitochondrial dynamics can cause various neurological diseases. Elucidation of mechanisms and applications involved in mitochondrial dynamics will inform the development of new therapeutic targets and strategies for neurological diseases. Dynamin-related protein 1 (Drp1), as a highly relevant molecular for mitochondrial dynamics, might be a potential target for treating neurological diseases in the future.

Indexed as

Alzeimer’s diseaseDrp1mitochondrial dynamicsmitochondrial fusion proteinParkinson’s disease

Identifiers

PMID37082676
PMCPMC10113088
OpenAlexW4319335369

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.