Evidence map›Paper›PMID 30632492›Full record

ReviewNeural regeneration research2019

Rescue axonal defects by targeting mitochondrial dynamics in hereditary spastic paraplegias.

Yongchao Mou, Xue-Jun Li

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2019. 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
0.8field-weighted citation impact, top 35% 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, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Clinical features and genotype in COQ4 associated hereditary spastic paraplegia: a case report and a literature reanalysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Importance of lipids for upper motor neuron health and disease.Seminars in cell & developmental biology · 2021
    Review
  11. Review
  12. Article
  13. 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

2 authors at 2 institutions in 1 country.

Yongchao MouDepartment of Biomedical Sciences, University of Illinois College of Medicine Rockford, Rockford; Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, USA.
Xue-Jun LiDepartment of Biomedical Sciences, University of Illinois College of Medicine Rockford, Rockford; Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, USA.
Illinois College · USUniversity of Illinois Chicago, Rockford campus · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired axonal development and degeneration underlie debilitating neurodegenerative diseases including hereditary spastic paraplegia, a large group of inherited diseases. Hereditary spastic paraplegia is caused by retrograde degeneration of the long corticospinal tract axons, leading to progressive spasticity and weakness of leg and hip muscles. There are over 70 subtypes with various underlying pathophysiological processes, such as defective vesicular trafficking, lipid metabolism, organelle shaping, axonal transport, and mitochondrial dysfunction. Although hereditary spastic paraplegia consists of various subtypes with different pathological characteristics, defects in mitochondrial morphology and function emerge as one of the common cellular themes in hereditary spastic paraplegia. Mitochondrial morphology and function are remodeled by mitochondrial dynamics regulated by several key fission and fusion mediators. However, the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia remains largely unknown. Recently, studies reported perturbed mitochondrial morphology in hereditary spastic paraplegia neurons. Moreover, downregulation of mitochondrial fission regulator dynamin-related protein 1, both pharmacologically and genetically, could rescue axonal outgrowth defects in hereditary spastic paraplegia neurons, providing a potential therapeutic target for treating these hereditary spastic paraplegia. This mini-review will describe the regulation of mitochondrial fission/fusion, the link between mitochondrial dynamics and axonal defects, and the recent progress on the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia.

Indexed as

axonal degenerationdynamin-related protein 1fissionfusionhereditary spastic paraplegiainduced pluripotent stem cellsmitochondrial dynamicsmitochondrial dysfunction

Identifiers

PMID30632492
PMCPMC6352593
OpenAlexW2909164413

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.