Evidence map›Paper›PMID 36061599›Full record

ReviewFrontiers in neuroscience2022

CHCHD2 and CHCHD10: Future therapeutic targets in cognitive disorder and motor neuron disorder.

Tianlin Jiang, Yanli Wang, Xiaohong Wang, Jun Xu

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Genetic and environmental risk factors of Parkinsonism.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mitochondrial stress response and myogenic differentiation.Frontiers in cell and developmental biology · 2024
    Review
  8. Article
  9. Article
  10. 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

4 authors.

Tianlin JiangInstitute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
Yanli WangDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Xiaohong WangInstitute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
Jun XuDepartment of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CHCHD2 and CHCHD10 are homolog mitochondrial proteins that play key roles in the neurological, cardiovascular, and reproductive systems. They are also involved in the mitochondrial metabolic process. Although previous research has concentrated on their functions within mitochondria, their functions within apoptosis, synaptic plasticity, cell migration as well as lipid metabolism remain to be concluded. The review highlights the different roles played by CHCHD2 and/or CHCHD10 binding to various target proteins (such as OPA-1, OMA-1, PINK, and TDP43) and reveals their non-negligible effects in cognitive impairments and motor neuron diseases. This review focuses on the functions of CHCHD2 and/or CHCHD10. This review reveals protective effects and mechanisms of CHCHD2 and CHCHD10 in neurodegenerative diseases characterized by cognitive and motor deficits, such as frontotemporal dementia (FTD), Lewy body dementia (LBD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). However, there are numerous specific mechanisms that have yet to be elucidated, and additional research into these mechanisms is required.

Indexed as

apoptosisCHCHD10CHCHD2cognitive impairmentmitochondriamotor neuron injury

Identifiers

PMID36061599
PMCPMC9434015

What OpenQuestion holds

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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.