Evidence map›Paper›PMID 28497982›Full record

ReviewAntioxidants & redox signaling2018

Neuroprotection in Oxidative Stress-Related Neurodegenerative Diseases: Role of Endocannabinoid System Modulation.

Janos Paloczi, Zoltan V Varga, George Hasko, Pal Pacher

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
6.9field-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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

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  18. Heteromers Formed by GPR55 and Either Cannabinoid CBInternational journal of molecular sciences · 2024
    Article
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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

4 authors at 1 institution in 1 country.

Janos Paloczi1 Laboratory of Cardiovascular Physiology and Tissue Injury (LCPTI), National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH) , Bethesda, Maryland.
Zoltan V Varga1 Laboratory of Cardiovascular Physiology and Tissue Injury (LCPTI), National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH) , Bethesda, Maryland.
George Hasko2 Department of Surgery, Rutgers New Jersey Medical School , Newark, New Jersey.
Pal Pacher1 Laboratory of Cardiovascular Physiology and Tissue Injury (LCPTI), National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH) , Bethesda, Maryland.
Rutgers, The State University of New Jersey · US

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
6 · The paper itself

Abstract

significanceRedox imbalance may lead to overproduction of reactive oxygen and nitrogen species (ROS/RNS) and subsequent oxidative tissue damage, which is a critical event in the course of neurodegenerative diseases. It is still not fully elucidated, however, whether oxidative stress is the primary trigger or a consequence in the process of neurodegeneration. Recent Advances: Increasing evidence suggests that oxidative stress is involved in the propagation of neuronal injury and consequent inflammatory response, which in concert promote development of pathological alterations characteristic of most common neurodegenerative diseases. CRITICAL ISSUES: Accumulating recent evidence also suggests that there is an important interplay between the lipid endocannabinoid system [ECS; comprising the main cannabinoid 1 and 2 receptors (CB1 and CB2), endocannabinoids, and their synthetic and metabolizing enzymes] and various key inflammatory and redox-dependent processes. FUTURE DIRECTIONS: Targeting the ECS to modulate redox state-dependent cell death and to decrease consequent or preceding inflammatory response holds therapeutic potential in a multitude of oxidative stress-related acute or chronic neurodegenerative disorders from stroke and traumatic brain injury to Alzheimer's and Parkinson's diseases and multiple sclerosis, just to name a few, which will be discussed in this overview. Antioxid. Redox Signal. 29, 75-108.

Indexed as

AnimalsEndocannabinoidsHumansNeurodegenerative DiseasesNeuroprotective AgentsOxidative StressReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2EndocannabinoidsNeuroprotective AgentsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2endocannabinoidfree radicalsinflammationneurodegenerationneuroprotectionoxidative/nitrative stress

Identifiers

PMID28497982
PMCPMC5984569
OpenAlexW2612728880

What OpenQuestion holds

Textmetadata
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.