Evidence map›Paper›PMID 24494187›Full record

ReviewRedox biology2014

Autophagy as an essential cellular antioxidant pathway in neurodegenerative disease.

Samantha Giordano, Victor Darley-Usmar, Jianhua Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed
20.4field-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

189 citing papers in PubMed, 361 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Investigating the efficacy, methods, and challenges of induced pluripotent stem cells (iPSC) therapy in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  16. Review
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  19. Reduction of the CaFrontiers in cellular neuroscience · 2025
    Review
  20. Article

129 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.

Samantha GiordanoCenter for Free Radical Biology, University of Alabama at Birmingham, United States ; Department of Pathology, University of Alabama at Birmingham, United States.
Victor Darley-UsmarCenter for Free Radical Biology, University of Alabama at Birmingham, United States ; Department of Pathology, University of Alabama at Birmingham, United States.
Jianhua ZhangCenter for Free Radical Biology, University of Alabama at Birmingham, United States ; Department of Pathology, University of Alabama at Birmingham, United States ; Department of Veterans Affairs, Birmingham VA Medical Center, United States.
University of Alabama at Birmingham · US

Funding

Sex hormones and arthritis in a long lived animal modelP30AG050886 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Daniel L Smith · 2015 to 2026
$11.3M
Alpha-synuclein degradation mechanismsR01NS064090 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHANG, JIANHUA · 2010 to 2014
$1.6M
NIA NIH HHS P30 AG050886NINDS NIH HHS R01 NS064090NINDS NIH HHS R01-NS064090
6 · The paper itself

Abstract

Oxidative stress including DNA damage, increased lipid and protein oxidation, are important features of aging and neurodegeneration suggesting that endogenous antioxidant protective pathways are inadequate or overwhelmed. Importantly, oxidative protein damage contributes to age-dependent accumulation of dysfunctional mitochondria or protein aggregates. In addition, environmental toxins such as rotenone and paraquat, which are risk factors for the pathogenesis of neurodegenerative diseases, also promote protein oxidation. The obvious approach of supplementing the primary antioxidant systems designed to suppress the initiation of oxidative stress has been tested in animal models and positive results were obtained. However, these findings have not been effectively translated to treating human patients, and clinical trials for antioxidant therapies using radical scavenging molecules such as α-tocopherol, ascorbate and coenzyme Q have met with limited success, highlighting several limitations to this approach. These could include: (1) radical scavenging antioxidants cannot reverse established damage to proteins and organelles; (2) radical scavenging antioxidants are oxidant specific, and can only be effective if the specific mechanism for neurodegeneration involves the reactive species to which they are targeted and (3) since reactive species play an important role in physiological signaling, suppression of endogenous oxidants maybe deleterious. Therefore, alternative approaches that can circumvent these limitations are needed. While not previously considered an antioxidant system we propose that the autophagy-lysosomal activities, may serve this essential function in neurodegenerative diseases by removing damaged or dysfunctional proteins and organelles.

Indexed as

AutophagyAgingAnimalsAntioxidantsAntiparkinson AgentsBrainClinical Trials as TopicDisease Models, AnimalDrug Evaluation, PreclinicalHumansLipid PeroxidationLysosomesNerve Tissue ProteinsNeurodegenerative DiseasesNeuroprotective AgentsOxidation-ReductionAntioxidantsAntiparkinson AgentsNerve Tissue ProteinsNeuroprotective AgentsOxidoreductasesPeroxynitrous Acid6-OHDA, 6-hydroxydopamineAnimal modelsAnti-oxidantsAutophagyCBZ, carbamazepineClinical trialscurcumin, (1E,6E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dioneEGCG, epigallocatechin gallateGSH, glutathioneHIF1α, hypoxia-inducible factor 1-alphaHNE, 4-hydroxynonenaliPSC, induced pluripotent stem cellsLRRK2, leucine-rich repeat kinase 2MDA, malondialdehydeMitochondrial dysfunctionMitoQ, mitochondrially-targeted coenzyme QMnSOD, manganese superoxide dismutaseMPP+, 1-methyl-4-phenylpyridiniumMPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydro pyridineNeuronsNrf2, Nuclear factor (erythroid-derived 2)-like 2Parkinson’s diseasePINK1, PTEN-induced putative kinase 1Protein aggregationrasagiline, N-propargyl-1-(R)-aminoindanReactive oxygen speciesRedox signalingROS/RNS, reactive oxygen and nitrogen speciesSelegiline, N-propargyl-methamphetamineSirt1, NAD-dependent deacetylast sirtuin-1SOD, superoxide dismutaseTFEB, transcription factor EBthe ADAGIO study, the Attenuation of Disease Progression with Azilect Given Once-daily) studythe DATATOP Study, the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism Studythe NET-PD network, the NINDS Exploratory Trials in Parkinson’s Disease (NET-PD) networkthe TEMPO Study, the TVP-1012 in Early Monotherapy for PD Outpatients StudyToxinsUCHL1, ubiquitin carboxyl-terminal hydrolase L1UPDRS, Unified Parkinson’s Disease Rating Scale

Identifiers

PMID24494187
PMCPMC3909266
OpenAlexW2058074769

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.