Evidence map›Paper›PMID 36306327›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

A small molecule M1 promotes optic nerve regeneration to restore target-specific neural activity and visual function.

Ngan Pan Bennett Au, Raza Chand, Gajendra Kumar, Pallavi Asthana, Wing Yip Tam, Kin Man Tang, Chi-Chiu Ko, Chi Him Eddie Ma

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-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

27 citing papers in PubMed, 42 citations in OpenAlex.

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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 1 institution in 1 country.

Ngan Pan Bennett AuDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.ORCID 0000-0003-0245-9096
Raza ChandDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.ORCID 0000-0003-4890-8475
Gajendra KumarDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.ORCID 0000-0002-7437-6743
Pallavi AsthanaDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.
Wing Yip TamDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.ORCID 0000-0001-9714-5879
Kin Man TangDepartment of Chemistry, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.
Chi-Chiu KoDepartment of Chemistry, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.ORCID 0000-0002-2426-3206
Chi Him Eddie MaDepartment of Neuroscience, City University of Hong Kong, Hong Kong Special Administrative Region (HKSAR), China.
City University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axon regeneration is an energy-demanding process that requires active mitochondrial transport. In contrast to the central nervous system (CNS), axonal mitochondrial transport in regenerating axons of the peripheral nervous system (PNS) increases within hours and sustains for weeks after injury. Yet, little is known about targeting mitochondria in nervous system repair. Here, we report the induction of sustained axon regeneration, neural activities in the superior colliculus (SC), and visual function recovery after optic nerve crush (ONC) by M1, a small molecule that promotes mitochondrial fusion and transport. We demonstrated that M1 enhanced mitochondrial dynamics in cultured neurons and accelerated in vivo axon regeneration in the PNS. Ex vivo time-lapse imaging and kymograph analysis showed that M1 greatly increased mitochondrial length, axonal mitochondrial motility, and transport velocity in peripheral axons of the sciatic nerves. Following ONC, M1 increased the number of axons regenerating through the optic chiasm into multiple subcortical areas and promoted the recovery of local field potentials in the SC after optogenetic stimulation of retinal ganglion cells, resulting in complete recovery of the pupillary light reflex, and restoration of the response to looming visual stimuli was detected. M1 increased the gene expression of mitochondrial fusion proteins and major axonal transport machinery in both the PNS and CNS neurons without inducing inflammatory responses. The knockdown of two key mitochondrial genes,

Indexed as

AxonsOptic Nerve InjuriesHumansMitochondrial ProteinsNerve CrushNerve RegenerationOptic NerveRetinal Ganglion CellsSciatic NerveSmall Molecule LibrariesMitochondrial ProteinsSmall Molecule Librariesaxon regenerationmitochondrial dynamicsoptic nerve crushperipheral nerve injuryvisual function recovery

Identifiers

PMID36306327
PMCPMC9636930
OpenAlexW4307475507

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.