Evidence map›Paper›PMID 33546471›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models.

JunHyuk Woo, Hyesun Cho, YunHee Seol, Soon Ho Kim, Chanhyeok Park, Ali Yousefian-Jazi, Seung Jae Hyeon, Junghee Lee, Hoon Ryu

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. System-level brain modeling.Frontiers in computational neuroscience · 2025
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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

9 authors at 3 institutions in 2 countries.

JunHyuk WooBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Hyesun ChoBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.ORCID 0000-0003-1254-768X
YunHee SeolBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Soon Ho KimBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Chanhyeok ParkBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Ali Yousefian-JaziBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Seung Jae HyeonBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.
Junghee LeeDepartment of Neurology, Boston University Alzheimer's Disease Center, Boston University School of Medicine, Boston, MA 02118, USA.
Hoon RyuBrain Science Institute, Korea Institute of Science and Technology, Seoul 02792, Korea.ORCID 0000-0001-6544-3732
Korea Institute of Brain Science · KRBoston University · USSeoul National University · KR

Funding

Modulation of neuronal atrophy in Huntington's diseaseR01NS109537 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEE, JUNGHEE · 2018 to 2022
$1.4M
NINDS NIH HHS R01 NS109537
6 · The paper itself

Abstract

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5'-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and Parkinson's disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Indexed as

Alzheimer’s diseaseamyotrophic lateral sclerosisantioxidantscomputational modelingHuntington’s diseasemitochondriaoxidative stressParkinson’s disease

Identifiers

PMID33546471
PMCPMC7913624
OpenAlexW3127718025

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.