Evidence map›Paper›PMID 35041139›Full record

ReviewMolecular neurobiology2022

Recent Investigations on Neurotransmitters' Role in Acute White Matter Injury of Perinatal Glia and Pharmacotherapies-Glia Dynamics in Stem Cell Therapy.

Narasimha M Beeraka, P R Hemanth Vikram, M V Greeshma, Chinnappa A Uthaiah, Tahani Huria, Junqi Liu, Pramod Kumar, Vladimir N Nikolenko, Kirill V Bulygin, Mikhail Y Sinelnikov and 2 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 8% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Role of astrocytes in the pathogenesis of perinatal brain injury.Molecular medicine (Cambridge, Mass.) · 2025
    Review
  5. Review
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

12 authors at 6 institutions in 6 countries.

Narasimha M BeerakaCancer Center, Department of Radiation Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, People's Republic of China.
P R Hemanth VikramDepartment of Pharmaceutical Chemistry, JSS Pharmacy College, Mysuru, Karnataka, India.
M V GreeshmaCenter of Excellence in Molecular Biology and Regenerative Medicine (CEMR), Department of Biochemistry, JSS Medical College, JSS Academy of Higher Education and Research (JSS AHER), Mysuru, Karnataka, India.
Chinnappa A UthaiahCenter of Excellence in Molecular Biology and Regenerative Medicine (CEMR), Department of Biochemistry, JSS Medical College, JSS Academy of Higher Education and Research (JSS AHER), Mysuru, Karnataka, India.
Tahani HuriaFaculty of Medicine, Benghazi University, Benghazi, Libya.
Junqi LiuCancer Center, Department of Radiation Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, People's Republic of China.
Pramod KumarDepartment of Pharmaceutical Analysis, National Institute of Pharmaceutical Education and Research (NIPER-Guwahati), SilaKatamur (Halugurisuk), Changsari, Kamrup, 781101, Assam, India.
Vladimir N NikolenkoDepartment of Human Anatomy, I. M. Sechenov First Moscow State Medical University (Sechenov University), St. Trubetskaya, 8, bld. 2, Moscow, 119991, Russia.
Kirill V BulyginDepartment of Human Anatomy, I. M. Sechenov First Moscow State Medical University (Sechenov University), St. Trubetskaya, 8, bld. 2, Moscow, 119991, Russia.
Mikhail Y SinelnikovDepartment of Human Anatomy, I. M. Sechenov First Moscow State Medical University (Sechenov University), St. Trubetskaya, 8, bld. 2, Moscow, 119991, Russia.
Olga SukochevaDiscipline of Health Sciences, College of Nursing and Health Sciences, Flinders University, Bedford Park, South Australia, 5042, Australia.
Ruitai FanCancer Center, Department of Radiation Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, People's Republic of China. fccfanrt@zzu.edu.cn.ORCID http://orcid.org/0000-0003-3401-4315
JSS Academy of Higher Education and Research · INSechenov University · RUFirst Affiliated Hospital of Zhengzhou University · CNFlinders University · AUNational Institute of Pharmaceutical Education and Research · INUniversity of Leicester · GB

Funding

National Natural Science Foundation of China 81700729
6 · The paper itself

Abstract

Periventricular leukomalacia (PVL) and cerebral palsy are two neurological disease conditions developed from the premyelinated white matter ischemic injury (WMI). The significant pathophysiology of these diseases is accompanied by the cognitive deficits due to the loss of function of glial cells and axons. White matter makes up 50% of the brain volume consisting of myelinated and non-myelinated axons, glia, blood vessels, optic nerves, and corpus callosum. Studies over the years have delineated the susceptibility of white matter towards ischemic injury especially during pregnancy (prenatal, perinatal) or immediately after child birth (postnatal). Impairment in membrane depolarization of neurons and glial cells by ischemia-invoked excitotoxicity is mediated through the overactivation of NMDA receptors or non-NMDA receptors by excessive glutamate influx, calcium, or ROS overload and has been some of the well-studied molecular mechanisms conducive to the injury of white matter. Expression of glutamate receptors (GluR) and transporters (GLT1, EACC1, and GST) has significant influence in glial and axonal-mediated injury of premyelinated white matter during PVL and cerebral palsy. Predominantly, the central premyelinated axons express extensive levels of functional NMDA GluR receptors to confer ischemic injury to premyelinated white matter which in turn invoke defects in neural plasticity. Several underlying molecular mechanisms are yet to be unraveled to delineate the complete pathophysiology of these prenatal neurological diseases for developing the novel therapeutic modalities to mitigate pathophysiology and premature mortality of newborn babies. In this review, we have substantially discussed the above multiple pathophysiological aspects of white matter injury along with glial dynamics, and the pharmacotherapies including recent insights into the application of MSCs as therapeutic modality in treating white matter injury.

Indexed as

Brain InjuriesCerebral PalsyLeukomalacia, PeriventricularWhite MatterCell- and Tissue-Based TherapyGlutamic AcidHumansInfantInfant, NewbornNeurogliaNeurotransmitter AgentsReceptors, GlutamateReceptors, N-Methyl-D-AspartateGlutamic AcidNeurotransmitter AgentsReceptors, GlutamateReceptors, N-Methyl-D-AspartateGlial dynamicsGlutamate transportersIschemic InjuryNeurodegenerationNMDA receptors (NMDAR)PVLStem cell therapy

Identifiers

PMID35041139
OpenAlexW4205380810

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.