Evidence map›Paper›PMID 31328155›Full record

ArticleScience advances2019

Excessive exosome release is the pathogenic pathway linking a lysosomal deficiency to generalized fibrosis.

Diantha van de Vlekkert, Jeroen Demmers, Xinh-Xinh Nguyen, Yvan Campos, Eda Machado, Ida Annunziata, Huimin Hu, Elida Gomero, Xiaohui Qiu, Antonella Bongiovanni and 2 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-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

49 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Mitochondrial proteostasis regulated by CRL5Communications biology · 2025
    Article
  7. Article
  8. Review
  9. Article
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  12. Review
  13. Review
  14. AAV-mediated gene therapy for sialidosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  15. Article
  16. Article
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  20. 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 4 institutions in 3 countries.

Diantha van de VlekkertDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.ORCID 0000-0001-7498-1292
Jeroen DemmersProteomics Center, Erasmus University Medical Center, Wytemaweg 80, 3015 CN, Rotterdam, Netherlands.ORCID 0000-0002-8757-9611
Xinh-Xinh NguyenDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
Yvan CamposDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Eda MachadoDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.ORCID 0000-0002-1048-8447
Ida AnnunziataDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Huimin HuDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Elida GomeroDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.ORCID 0000-0001-9980-9042
Xiaohui QiuDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Antonella BongiovanniInstitute of Biomedicine and Molecular Immunology (IBIM), National Research Council (CNR) of Italy, Palermo, Italy.ORCID 0000-0002-0307-4043
Carol A Feghali-BostwickDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.ORCID 0000-0002-6750-6407
Alessandra d'AzzoDepartment of Genetics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.ORCID 0000-0003-1747-7502
St. Jude Children's Research Hospital · USMedical University of South Carolina · USErasmus MC · NLIstituto di Biomedicina e di Immunologia Molecolare Alberto Monroy · IT

Funding

Gene Transfer for Galactosialidosis - ResubR01DK095169 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI D'AZZO, ALESSANDRA · 2013 to 2016
$2.8M
Excessive Lysosomal Exocytosis Triggers Pathogenic Mechanisms in Sialidosis MiceR01GM104981 · NIGMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI D'AZZO, ALESSANDRA · 2013 to 2017
$1.4M
NIDDK NIH HHS R01 DK095169NIGMS NIH HHS R01 GM104981
6 · The paper itself

Abstract

Lysosomal exocytosis is a ubiquitous process negatively regulated by neuraminidase 1 (NEU1), a sialidase mutated in the glycoprotein storage disease sialidosis. In

Indexed as

Disease SusceptibilitySignal TransductionAnimalsbeta CateninBiomarkersDependovirusDisease Models, AnimalExocytosisExosomesFibroblastsFibrosisGenetic TherapyGene Transfer TechniquesHumansImmunohistochemistryLysosomesbeta CateninBiomarkersTransforming Growth Factor betaWnt Proteins

Identifiers

PMID31328155
PMCPMC6636989
OpenAlexW2957421097

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.