Evidence map›Paper›PMID 22942700›Full record

ArticleInternational journal of molecular sciences2012

The neuroprotective functions of transforming growth factor beta proteins.

Arpád Dobolyi, Csilla Vincze, Gabriella Pál, Gábor Lovas

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 5% 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

145 citing papers in PubMed, 2 syntheses or guidelines pooled it, 252 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
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  13. The meningeal-cerebellar axis: a new perspective on cerebellar development.Cellular and molecular life sciences : CMLS · 2025
    Review
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  15. Article
  16. Differential Roles of Neuro-Inflammatory Regulator, MAPK11 in Cortex and Hippocampus Following Post-Stroke Cognitive Impairments in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  17. Transforming Growth Factor-β Serum Levels Associated with Social Function in Subjects at Ultra-high Risk for Psychosis: A Multicenter Study.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
    Article
  18. Article
  19. Article
  20. Review

85 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 2 institutions in 1 country.

Arpád DobolyiDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tuzolto u. 58, Budapest H-1094, Hungary.
Csilla VinczeDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tuzolto u. 58, Budapest H-1094, Hungary.
Gabriella PálDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tuzolto u. 58, Budapest H-1094, Hungary.
Gábor LovasDepartment of Neurology, Semmelweis University, Balassa u. 6, Budapest H-1083, Hungary.
Hungarian Academy of Sciences · HUJahn Ferenc Dél-Pesti Kórház és Rendelőintézet · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor beta (TGF-β) proteins are multifunctional cytokines whose neural functions are increasingly recognized. The machinery of TGF-β signaling, including the serine kinase type transmembrane receptors, is present in the central nervous system. However, the 3 mammalian TGF-β subtypes have distinct distributions in the brain suggesting different neural functions. Evidence of their involvement in the development and plasticity of the nervous system as well as their functions in peripheral organs suggested that they also exhibit neuroprotective functions. Indeed, TGF-β expression is induced following a variety of types of brain tissue injury. The neuroprotective function of TGF-βs is most established following brain ischemia. Damage in experimental animal models of global and focal ischemia was shown to be attenuated by TGF-βs. In addition, support for their neuroprotective actions following trauma, sclerosis multiplex, neurodegenerative diseases, infections, and brain tumors is also accumulating. The review will also describe the potential mechanisms of neuroprotection exerted by TGF-βs including anti-inflammatory, -apoptotic, -excitotoxic actions as well as the promotion of scar formation, angiogenesis, and neuroregeneration. The participation of these mechanisms in the neuroprotective effects of TGF-βs during different brain lesions will also be discussed.

Indexed as

AnimalsApoptosisBrain NeoplasmsEncephalomyelitis, Autoimmune, ExperimentalHumansNerve RegenerationNeurodegenerative DiseasesNeuroprotective AgentsSignal TransductionTransforming Growth Factor betaNeuroprotective AgentsTransforming Growth Factor betabrain injurylesionneurodegenerationneuroprotectionstrokeTGF-β

Identifiers

PMID22942700
PMCPMC3430231
OpenAlexW2128640727

What OpenQuestion 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 OpenQuestion graph.