Evidence map›Paper›PMID 32579130›Full record

ArticleAging2020

Increased expression of connexin 43 in a mouse model of spinal motoneuronal loss.

Federica Maria Spitale, Nunzio Vicario, Michelino Di Rosa, Daniele Tibullo, Michele Vecchio, Rosario Gulino, Rosalba Parenti

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. International journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. The Role of Epigenetics in Neuroinflammatory-Driven Diseases.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

7 authors at 2 institutions in 1 country.

Federica Maria SpitaleDepartment of Biomedical and Biotechnological Sciences, Section of Physiology, University of Catania, Catania 95123, Italy.
Nunzio VicarioDepartment of Biomedical and Biotechnological Sciences, Section of Physiology, University of Catania, Catania 95123, Italy.
Michelino Di RosaDepartment of Biomedical and Biotechnological Sciences, Section of Anatomy, Histology and Movement Sciences, University of Catania, Catania 95123, Italy.
Daniele TibulloDepartment of Biomedical and Biotechnological Sciences, Section of Biochemistry, University of Catania, Catania 95123, Italy.
Michele VecchioDepartment of Biomedical and Biotechnological Sciences, Section of Pharmacology, University of Catania, Catania 95123, Italy.
Rosario GulinoDepartment of Biomedical and Biotechnological Sciences, Section of Physiology, University of Catania, Catania 95123, Italy.
Rosalba ParentiDepartment of Biomedical and Biotechnological Sciences, Section of Physiology, University of Catania, Catania 95123, Italy.
University of Catania · ITAzienda Ospedaliero-Universitaria Policlinico - Vittorio Emanuele · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is one of the most common motoneuronal disease, characterized by motoneuronal loss and progressive paralysis. Despite research efforts, ALS remains a fatal disease, with a survival of 2-5 years after disease onset. Numerous gene mutations have been correlated with both sporadic (sALS) and familiar forms of the disease, but the pathophysiological mechanisms of ALS onset and progression are still largely uncertain. However, a common profile is emerging in ALS pathological features, including misfolded protein accumulation and a cross-talk between neuroinflammatory and degenerative processes. In particular, astrocytes and microglial cells have been proposed as detrimental influencers of perineuronal microenvironment, and this role may be exerted via gap junctions (GJs)- and hemichannels (HCs)-mediated communications. Herein we investigated the role of the main astroglial GJs-forming connexin, Cx43, in human ALS and the effects of focal spinal cord motoneuronal depletion onto the resident glial cells and Cx43 levels. Our data support the hypothesis that motoneuronal depletion may affect glial activity, which in turn results in reactive Cx43 expression, further promoting neuronal suffering and degeneration.

Indexed as

Amyotrophic Lateral SclerosisSpinal CordAdultAnimalsAstrocytesConnexin 43Disease Models, AnimalFemaleGap JunctionsGlial Fibrillary Acidic ProteinHumansMaleMiceMiddle AgedMotor NeuronsConnexin 43GFAP protein, humanGJA1 protein, humanGJA1 protein, mouseGlial Fibrillary Acidic ProteinALSastrocytegap junctionneurodegenerationneuronal loss

Identifiers

PMID32579130
PMCPMC7377853
OpenAlexW3037590921

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.