Evidence map›Paper›PMID 35429433›Full record

ReviewNeuron2022

Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration.

Xiu-Tang Cheng, Ning Huang, Zu-Hang Sheng

Open access · greenAbstract readReview
In one paragraph

Review in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
19.8field-weighted citation impact, top 1% 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

135 citing papers in PubMed, 221 citations in OpenAlex.

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75 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Xiu-Tang ChengSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2B-215, 35 Convent Drive, Bethesda, MD 20892-3706, USA.
Ning HuangSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2B-215, 35 Convent Drive, Bethesda, MD 20892-3706, USA.
Zu-Hang ShengSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2B-215, 35 Convent Drive, Bethesda, MD 20892-3706, USA. Electronic address: shengz@ninds.nih.gov.
National Institutes of Health · US

Funding

Regulation of mitochondrial transport and its impact on synaptic transmissionZIANS003029 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$31.5M
Transport and regulation of presynaptic release machineryZIANS002946 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$25.6M
Transport and regulation of presynaptic release machineryZ01NS002946 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 1997 to 2008
$2.1M
Axonal mitochondrial mobility and its impact on synaptic transmissionZ01NS003029 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2007 to 2008
$2.1M
Intramural NIH HHS Z01 NS002946Intramural NIH HHS Z01 NS003029Intramural NIH HHS ZIA NS002946Intramural NIH HHS ZIA NS003029
6 · The paper itself

Abstract

Mitochondria generate ATP essential for neuronal growth, function, and regeneration. Due to their polarized structures, neurons face exceptional challenges to deliver mitochondria to and maintain energy homeostasis throughout long axons and terminal branches where energy is in high demand. Chronic mitochondrial dysfunction accompanied by bioenergetic failure is a pathological hallmark of major neurodegenerative diseases. Brain injury triggers acute mitochondrial damage and a local energy crisis that accelerates neuron death. Thus, mitochondrial maintenance defects and axonal energy deficits emerge as central problems in neurodegenerative disorders and brain injury. Recent studies have started to uncover the intrinsic mechanisms that neurons adopt to maintain (or reprogram) axonal mitochondrial density and integrity, and their bioenergetic capacity, upon sensing energy stress. In this review, we discuss recent advances in how neurons maintain a healthy pool of axonal mitochondria, as well as potential therapeutic strategies that target bioenergetic restoration to power neuronal survival, function, and regeneration.

Indexed as

Brain InjuriesNeurodegenerative DiseasesAxonsEnergy MetabolismHumansMitochondriaRegenerationaxonal transportbioenergetic failurebrain injuryenergy deficitsenergy metabolismenergy recoveryischemiamitochondrial anchoringmitochondrial quality controlneurodegeneration

Identifiers

PMID35429433
PMCPMC9233091
OpenAlexW4224043064

What OpenQuestion holds

Textmetadata
LicenceTDM
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.