Evidence map›Paper›PMID 33389706›Full record

ReviewPharmacological reports : PR2021

Neuroprotection through G-CSF: recent advances and future viewpoints.

Vikrant Rahi, Sumit Jamwal, Puneet Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmacological reports : PR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.9field-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

23 citing papers in PubMed, 48 citations in OpenAlex.

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  9. The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024
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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

3 authors at 3 institutions in 2 countries.

Vikrant RahiDepartment of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, India.
Sumit JamwalDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT, 06511, USA.
Puneet KumarDepartment of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, India. punnubansal79@gmail.com.ORCID http://orcid.org/0000-0002-7978-1043
Central University of Punjab · INMaharaja Ranjit Singh Punjab Technical University · INYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Granulocyte-colony stimulating factor (G-CSF), a member of the cytokine family of hematopoietic growth factors, is 19.6 kDa glycoprotein which is responsible for the proliferation, maturation, differentiation, and survival of neutrophilic granulocyte lineage. Apart from its proven clinical application to treat chemotherapy-associated neutropenia, recent pre-clinical studies have highlighted the neuroprotective roles of G-CSF i.e., mobilization of haemopoietic stem cells, anti-apoptotic, neuronal differentiation, angiogenesis and anti-inflammatory in animal models of neurological disorders. G-CSF is expressed by numerous cell types including neuronal, immune and endothelial cells. G-CSF is released in autocrine manner and binds to its receptor G-CSF-R which further activates numerous signaling transduction pathways including PI3K/AKT, JAK/STAT and MAP kinase, and thereby promote neuronal survival, proliferation, differentiation, mobilization of hematopoietic stem and progenitor cells. The expression of G-CSF receptors (G-CSF-R) in the different brain regions and their upregulation in response to neuronal insult indicates the autocrine protective signaling mechanism of G-CSF by inhibition of apoptosis, inflammation, and stimulation of neurogenesis. These observed neuroprotective effects of G-CSF makes it an attractive target to mitigate neurodegeneration associated with neurological disorders. The objective of the review is to highlight and summarize recent updates on G-CSF as a therapeutically versatile neuroprotective agent along with mechanisms of action as well as possible clinical applications in neurodegenerative disorders including AD, PD and HD.

Indexed as

AnimalsApoptosisGranulocyte Colony-Stimulating FactorHumansInflammationNeurodegenerative DiseasesNeuronsNeuroprotective AgentsReceptors, Granulocyte Colony-Stimulating FactorSignal TransductionGranulocyte Colony-Stimulating FactorNeuroprotective AgentsReceptors, Granulocyte Colony-Stimulating FactorAlzheimer’s diseaseGranulocyte-colony stimulating factorGranulocyte-colony stimulating factor-receptorsHuntington’s diseaseNeuroprotectionParkinson’s disease

Identifiers

PMID33389706
OpenAlexW3118259724

What Socratic 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 Socratic graph.