Evidence map›Paper›PMID 30576920›Full record

ReviewRedox biology2019

NRF2 and NF-қB interplay in cerebrovascular and neurodegenerative disorders: Molecular mechanisms and possible therapeutic approaches.

Farzane Sivandzade, Shikha Prasad, Aditya Bhalerao, Luca Cucullo

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 351 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
351citing papers in PubMed, 1 pooled it
17.0field-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

351 citing papers in PubMed, 1 synthesis or guideline pooled it, 606 citations in OpenAlex.

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291 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

4 authors at 3 institutions in 1 country.

Farzane SivandzadeDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA. Electronic address: farzane.sivandzade@ttuhsc.edu.
Shikha PrasadDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: Shikha.Prasad@northwestern.edu.
Aditya BhaleraoDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA. Electronic address: aditya.bhalerao@ttuhsc.edu.
Luca CuculloDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA; Center for Blood Brain Barrier Research, Texas Tech University Health Sciences Center, Amarillo, TX 79106, USA. Electronic address: luca.cucullo@ttuhsc.edu.
Texas Tech University · USNorthwestern University · USTexas Tech University Health Sciences Center · US

Funding

Testing tobacco smoke toxicity at the blood-brain barrierR01DA029121 · NIDA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI ABBRUSCATO, THOMAS J, CUCULLO, LUCA · 2011 to 2021
$3.6M
NIDA NIH HHS R01 DA029121
6 · The paper itself

Abstract

Electrophiles and reactive oxygen species (ROS) play a major role in modulating cellular defense mechanisms as well as physiological functions, and intracellular signaling. However, excessive ROS generation (endogenous and exogenous) can create a state of redox imbalance leading to cellular and tissue damage (Ma and He, 2012) [1]. A growing body of research data strongly suggests that imbalanced ROS and electrophile overproduction are among the major prodromal factors in the onset and progression of several cerebrovascular and neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), stroke, Alzheimer's disease (AD), Parkinson's disease (PD), and aging (Ma and He, 2012; Ramsey et al., 2017; Salminen et al., 2012; Sandberg et al., 2014; Sarlette et al., 2008; Tanji et al., 2013) [1-6]. Cells offset oxidative stress by the action of housekeeping antioxidative enzymes (such as superoxide dismutase, catalase, glutathione peroxidase) as well direct and indirect antioxidants (Dinkova-Kostova and Talalay, 2010) [7]. The DNA sequence responsible for modulating the antioxidative and cytoprotective responses of the cells has been identified as the antioxidant response element (ARE), while the nuclear factor erythroid 2-related factor (NRF2) is the major regulator of the xenobiotic-activated receptor (XAR) responsible for activating the ARE-pathway, thus defined as the NRF2-ARE system (Ma and He, 2012) [1]. In addition, the interplay between the NRF2-ARE system and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB, a protein complex that controls cytokine production and cell survival), has been further investigated in relation to neurodegenerative and neuroinflammatory disorders. On these premises, we provide a review analysis of current understanding of the NRF2-NF-ĸB interplay, their specific role in major CNS disorders, and consequent therapeutic implication for the treatment of neurodegenerative and cerebrovascular diseases.

Indexed as

Disease SusceptibilityAgingAnimalsCerebrovascular DisordersHumansHyperglycemiaInflammationMolecular Targeted TherapyNeurodegenerative DiseasesNF-E2-Related Factor 2NF-kappa BOxidative StressReactive Oxygen SpeciesSignal TransductionSmokingNF-E2-Related Factor 2NF-kappa BReactive Oxygen SpeciesAlternativeAntioxidativeCerebrovascularCytoprotection NeurodegenerativeInflammationNf-κBOxidative stress

Identifiers

PMID30576920
PMCPMC6302038
OpenAlexW2903380994

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.