Evidence map›Paper›PMID 33653014›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress.

Nadia Sadanandan, Blaise Cozene, You Jeong Park, Jeffrey Farooq, Chase Kingsbury, Zhen-Jie Wang, Alexa Moscatello, Madeline Saft, Justin Cho, Bella Gonzales-Portillo and 1 more

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 17 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

11 authors at 1 institution in 1 country.

Nadia SadanandanDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.ORCID 0000-0001-8826-5043
Blaise CozeneDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
You Jeong ParkDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Jeffrey FarooqDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.ORCID 0000-0002-6507-6626
Chase KingsburyDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Zhen-Jie WangDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Alexa MoscatelloDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.ORCID 0000-0002-2755-0083
Madeline SaftDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Justin ChoDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Bella Gonzales-PortilloDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
Cesar V BorlonganDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, Florida 33612, USA.
University of South Florida · US

Funding

NIH HHS NIH R01NS090962, NIH R01NS102395, and NIH R21NS109575
6 · The paper itself

Abstract

Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body's endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. The overproduction of ROS compromises the functional and structural integrity of brain tissue. Therefore, it is essential to investigate the mechanisms involved in oxidative stress to help obtain adequate treatment options for stroke. Here, we focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.

Indexed as

antioxidantcell signalingneurodegenerationoxidative stresspituitary adenylate cyclase-activating polypeptidesreactive oxygen speciesstroke

Identifiers

PMID33653014
PMCPMC7996859
OpenAlexW3135523028

What Socratic 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 Socratic graph.