Evidence map›Paper›PMID 36910151›Full record

ReviewFrontiers in cell and developmental biology2023

Dysregulated proteostasis network in neuronal diseases.

Ching-San Tseng, Yu-Wen Chao, Yi-Hsiang Liu, Yi-Shuian Huang, Hsu-Wen Chao

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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  13. Cell type-specific gene therapy confers protection against motor neuron disease caused by a TFG variant.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

5 authors.

Ching-San TsengDepartment of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Yu-Wen ChaoDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Yi-Hsiang LiuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Yi-Shuian HuangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Hsu-Wen ChaoDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term maintenance of synaptic connections is important for brain function, which depends on varying proteostatic regulations to govern the functional integrity of neuronal proteomes. Proteostasis supports an interconnection of pathways that regulates the fate of proteins from synthesis to degradation. Defects in proteostatic signaling are associated with age-related functional decline and neurodegenerative diseases. Recent studies have advanced our knowledge of how cells have evolved distinct mechanisms to safely control protein homeostasis during synthesis, folding and degradation, and in different subcellular organelles and compartments. Neurodegeneration occurs when these protein quality controls are compromised by accumulated pathogenic proteins or aging to an irreversible state. Consequently, several therapeutic strategies, such as targeting the unfolded protein response and autophagy pathways, have been developed to reduce the burden of misfolded proteins and proved useful in animal models. Here, we present a brief overview of the molecular mechanisms involved in maintaining proteostatic networks, along with some examples linking dysregulated proteostasis to neuronal diseases.

Indexed as

mRNA translationneurodegenerationpost-translation modificationprotein degradationstress granule

Identifiers

PMID36910151
PMCPMC9998692

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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.