Evidence map›Paper›PMID 29951942›Full record

ArticleMolecular neurobiology2019

Photobiomodulation for Global Cerebral Ischemia: Targeting Mitochondrial Dynamics and Functions.

Ruimin Wang, Yan Dong, Yujiao Lu, Wenli Zhang, Darrell W Brann, Quanguang Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
6.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 89 citations in OpenAlex.

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  19. Photobiomodulation for Neurodegenerative Diseases: A Scoping Review.International journal of molecular sciences · 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

6 authors at 2 institutions in 2 countries.

Ruimin WangNeurobiology Institute of Medical Research Center, North China University of Science and Technology, Tangshan, 063000, China. minruiwang@gmail.com.
Yan DongDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA.
Yujiao LuDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA.
Wenli ZhangNeurobiology Institute of Medical Research Center, North China University of Science and Technology, Tangshan, 063000, China.
Darrell W BrannDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA. dbrann@augusta.edu.
Quanguang ZhangDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA. qzhang@augusta.edu.ORCID http://orcid.org/0000-0001-6499-7952
Augusta University · USNorth China University of Science and Technology · CN

Funding

Brain Aromatase in Neurological Function and DiseaseR01NS088058 · NINDS · AUGUSTA UNIVERSITY · PI BRANN, DARRELL W, VADLAMUDI, RATNA K · 2015 to 2019
$1.8M
Low-level Laser Therapy in Global Cerebral IschemiaR01NS086929 · NINDS · AUGUSTA UNIVERSITY · PI ZHANG, QUANGUANG · 2014 to 2018
$1.7M
NINDS NIH HHS NS086929NINDS NIH HHS R01 NS086929NINDS NIH HHS R01 NS088058
6 · The paper itself

Abstract

Hypothermia is currently the only approved therapy for global cerebral ischemia (GCI) after cardiac arrest; however, it unfortunately has multiple adverse effects. As a noninvasive procedure, photobiomodulation (PBM) therapy has emerged as a potential novel treatment for brain injury. PBM involves the use of low-level laser light therapy to influence cell behavior. In this study, we evaluated the therapeutic effects of PBM treatment with an 808-nm diode laser initiated 6 h after GCI. It was noted that PBM dose-dependently protected against GCI-induced neuronal death in the vulnerable hippocampal CA1 subregion. Functional assessments demonstrated that PBM markedly preserved both short-term (a week) and long-term (6 months) spatial learning and memory function following GCI. Further mechanistic studies revealed that PBM post-treatment (a) preserved healthy mitochondrial dynamics and suppressed substantial mitochondrial fragmentation of CA1 neurons, by reducing the detrimental Drp1 GTPase activity and its interactions with adaptor proteins Mff and Fis1 and by balancing mitochondrial targeting fission and fusion protein levels; (b) reduced mitochondrial oxidative damage and excessive mitophagy and restored mitochondrial overall health status and preserved mitochondrial function; and (c) suppressed mitochondria-dependent apoptosome formation/caspase-3/9 apoptosis-processing activities. Additionally, we validated, in an in vitro ischemia model, that cytochrome c oxidase served as a key PBM target for mitochondrial function preservation and neuroprotection. Our findings suggest that PBM serves as a promising therapeutic strategy for the functional recovery after GCI, with mechanisms involving PBM's preservation on mitochondrial dynamics and functions and the inhibition of delayed apoptotic neuronal death in GCI.

Indexed as

Low-Level Light TherapyAnimalsBrain IschemiaCell DeathHippocampusMaleMaze LearningMitochondriaMitochondrial DynamicsNeuronsRatsRats, Sprague-DawleyApoptosisCognitionGlobal cerebral ischemiaMitochondrial dysfunctionPhotobiomodulation therapy

Identifiers

PMID29951942
PMCPMC6310117
OpenAlexW2811243461

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.