Evidence map›Paper›PMID 29097102›Full record

ReviewTrends in endocrinology and metabolism: TEM2017

'SNO'-Storms Compromise Protein Activity and Mitochondrial Metabolism in Neurodegenerative Disorders.

Tomohiro Nakamura, Stuart A Lipton

Abstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.7field-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

40 citing papers in PubMed, 59 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

2 authors at 2 institutions in 1 country.

Tomohiro NakamuraNeuroscience Translational Center, and Departments of Molecular Medicine and Neuroscience, The Scripps Research Institute, La Jolla, CA 92037, USA; Neurodegenerative Disease Center, Scintillon Institute, San Diego, CA 92121, USA. Electronic address: tnakamura@scripps.edu.
Stuart A LiptonNeuroscience Translational Center, and Departments of Molecular Medicine and Neuroscience, The Scripps Research Institute, La Jolla, CA 92037, USA; Neurodegenerative Disease Center, Scintillon Institute, San Diego, CA 92121, USA; Department of Neurosciences, University of California San Diego, School of Medicine, La Jolla, CA 92093, USA. Electronic address: slipton@scripps.edu.
Scintillon Institute · USScripps Research Institute · US

Funding

PROJECT III - GENETIC APPROACH TO EXCITATORY TRANSMISSIONP01HD029587 · NICHD · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 1992 to 2016
$21.9M
Novel Proteomics Approach to HIV-Associated Neurocognitive Disorder & Drug AbuseDP1DA041722 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI LIPTON, STUART A · 2016 to 2020
$7.0M
Project-002P30NS076411 · NINDS · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 2011 to 2016
$4.5M
Dynamic Interactions of the S-Nitrosoproteome in Type 2 Diabetes/Metabolic Syndrome and Alzheimer’s DiseaseRF1AG057409 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI LIPTON, STUART A · 2017 to 2020
$4.1M
S-Nitrosylation-Induced Posttranslational Modification and Aberrant Cell Signaling in Sporadic Alzheimer's DiseaseR01AG056259 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI LIPTON, STUART A · 2017 to 2021
$3.3M
Modeling Parkinson's Disease with Isogenic hiPSC-Derived Dopaminergic NeuronsR01NS086890 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI LIPTON, STUART A · 2014 to 2018
$2.1M
NIA NIH HHS R01 AG056259NIA NIH HHS RF1 AG057409NICHD NIH HHS P01 HD029587NIDA NIH HHS DP1 DA041722NINDS NIH HHS P30 NS076411NINDS NIH HHS R01 NS086890
6 · The paper itself

Abstract

The prevalence of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), is currently a major public health concern due to the lack of efficient disease-modifying therapeutic options. Recent evidence suggests that mitochondrial dysfunction and nitrosative/oxidative stress are key common mediators of pathogenesis. In this review, we highlight molecular mechanisms linking NO-dependent post-translational modifications, such as cysteine S-nitrosylation and tyrosine nitration, to abnormal mitochondrial metabolism. We further discuss the hypothesis that pathological levels of NO compromise brain energy metabolism via aberrant S-nitrosylation of key enzymes in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation, contributing to neurodegenerative conditions. A better understanding of these pathophysiological events may provide a potential pathway for designing novel therapeutics to ameliorate neurodegenerative disorders.

Indexed as

AnimalsCitric Acid CycleElectron TransportEnergy MetabolismHumansMitochondriaNeurodegenerative DiseasesOxidation-Reductionelectron transport chainmitochondrial metabolitesneurodegenerationnitrationS-nitrosylationtricarboxylic acid cycle

Identifiers

PMID29097102
PMCPMC5701818
OpenAlexW2766367771

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.