Evidence map›Paper›PMID 30377983›Full record

ReviewMolecular neurobiology2019

Astrocytes and the TGF-β1 Pathway in the Healthy and Diseased Brain: a Double-Edged Sword.

Luan Pereira Diniz, Isadora Matias, Michele Siqueira, Joice Stipursky, Flávia Carvalho Alcantara Gomes

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

92 citing papers in PubMed, 164 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Pain Hypersensitivity in a Mouse Model of Marfan Syndrome.Antioxidants (Basel, Switzerland) · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

32 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

5 authors at 1 institution in 1 country.

Luan Pereira DinizInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Isadora MatiasInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Michele SiqueiraInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Joice StipurskyInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
Flávia Carvalho Alcantara GomesInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil. fgomes@icb.ufrj.br.
Universidade Federal do Rio de Janeiro · BR

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico .Coordenação de Aperfeiçoamento de Pessoal de Nível Superior .Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro ..Ministério da Saúde .
6 · The paper itself

Abstract

Transforming growth factor betas (TGF-βs) are known as multifunctional growth factors that participate in the regulation of key events of development, disease, and tissue repair. In the brain, TGF-β1 has been widely recognized as an injury-related cytokine, particularly associated with astrocyte scar formation in response to brain injury. In the last decade, however, evidence has indicated that in addition to its role in brain injury, TGF-β1 might be a crucial regulator of cell survival and differentiation, brain homeostasis, angiogenesis, memory formation, and neuronal plasticity. In this review, we will discuss the emerging scenario of TGF-β1 as a key regulator of astrocyte differentiation and function and the implications of TGF-β1 as a novel mediator of cellular interactions in the central nervous system. First, we will discuss the cellular and molecular basis underlying the effect of TGF-β on astrocyte generation and its impact on angiogenesis and blood-brain barrier function. Then, we will focus on the role of astrocytes in the development and remodeling of synapses and the role of TGF-β1 as a new mediator of these events. Furthermore, we present seminal data that contributed to the emerging concept that astrocyte dysfunction might be associated with neurodegenerative diseases, with a special focus on Alzheimer's disease, and discuss the pros and cons of TGF-β signaling deficits in these processes. Finally, we argue that understanding how astrocytic signals, such as TGF-β1, regulate brain function might offer new insights into human learning, memory, and cognition, and ultimately, this understanding may provide new targets for the treatment of neurological diseases.

Indexed as

AgingAnimalsAstrocytesBrainBrain DiseasesHumansNeovascularization, PhysiologicTransforming Growth Factor beta1Transforming Growth Factor beta1Alzheimer’s diseaseAngiogenesisAstrocyteRadial gliaSynapseTGF-β1

Identifiers

PMID30377983
OpenAlexW2898726539

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.