Evidence map›Paper›PMID 39044100›Full record

ArticleThe EMBO journal2024

Connexin43 promotes exocytosis of damaged lysosomes through actin remodelling.

Neuza Domingues, Steve Catarino, Beatriz Cristóvão, Lisa Rodrigues, Filomena A Carvalho, Maria João Sarmento, Mónica Zuzarte, Jani Almeida, Teresa Ribeiro-Rodrigues, Ânia Correia-Rodrigues and 9 more

Abstract read
In one paragraph

Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Metabolic Imaging and Molecular Signatures Reveal Metabolic Phenotypes in Recurrent Glioblastoma.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Article
  4. Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025
    Review
  11. Article
  12. Article
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

19 authors.

Neuza DominguesUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.
Steve CatarinoUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0000-0001-9644-6960
Beatriz CristóvãoUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.
Lisa RodriguesUniv Coimbra, Center for Neurosciences and Cell Biology (CNC), Coimbra, Portugal.ORCID http://orcid.org/0000-0001-9898-2409
Filomena A CarvalhoInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.ORCID http://orcid.org/0000-0001-6088-3894
Maria João SarmentoInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.ORCID http://orcid.org/0000-0003-1765-4724
Mónica ZuzarteUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.
Jani AlmeidaUniv Coimbra, Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0000-0003-2024-0434
Teresa Ribeiro-RodriguesUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0000-0002-5169-6090
Ânia Correia-RodriguesUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0009-0000-5701-1585
Fábio FernandesInstitute for Bioengineering and Biosciences (IBB) and Associate Laboratory i4HB-Institute for Health and Bioeconomy, Department of Bioengineering, Instituto Superior Técnico, Universidade de Lisboa, Lisbon, Portugal.
Paulo Rodrigues-SantosUniv Coimbra, Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0000-0001-7519-1620
Trond AasenVall d'Hebron Research Institute (VHIR), Barcelona, Spain.ORCID http://orcid.org/0000-0003-0763-2695
Nuno C SantosInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Viktor I KorolchukBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Teresa GonçalvesUniv Coimbra, Faculty of Medicine, Coimbra, Portugal.ORCID http://orcid.org/0000-0001-9347-0535
Ira MilosevicMultidisciplinary Institute of Ageing, University of Coimbra, Coimbra, Portugal.
Nuno RaimundoMultidisciplinary Institute of Ageing, University of Coimbra, Coimbra, Portugal.ORCID http://orcid.org/0000-0002-5988-9129
Henrique GirãoUniv Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal. hmgirao@fmed.uc.pt.ORCID http://orcid.org/0000-0002-5786-8447

Funding

EC | European Regional Development Fund (ERDF) Comissão de Coordenação e Desenvolvimento Regional do Centro - CCDRC through the Centro2020 ProgrammEC | Horizon 2020 Framework Programme (H2020) 857524'la Caixa' Foundation ('la Caixa') Synageing HR22-00854MEC | Fundação para a Ciência e a Tecnologia (FCT) FCT-2022.09311MEC | Fundação para a Ciência e a Tecnologia (FCT) FCT-PTDC/MED-NEU/8030/2020MEC | Fundação para a Ciência e a Tecnologia (FCT) PPBI-POCI-01-0145-FEDER-022122MEC | Fundação para a Ciência e a Tecnologia (FCT) UIDB/04539/2020MEC | Fundação para a Ciência e a Tecnologia (FCT) UIDP/04539/2020Wellcome TrustWellcome Trust (WT) 224361/Z/21/Z
6 · The paper itself

Abstract

A robust and efficient cellular response to lysosomal membrane damage prevents leakage from the lysosome lumen into the cytoplasm. This response is understood to happen through either lysosomal membrane repair or lysophagy. Here we report exocytosis as a third response mechanism to lysosomal damage, which is further potentiated when membrane repair or lysosomal degradation mechanisms are impaired. We show that Connexin43 (Cx43), a protein canonically associated with gap junctions, is recruited from the plasma membrane to damaged lysosomes, promoting their secretion and accelerating cell recovery. The effects of Cx43 on lysosome exocytosis are mediated by a reorganization of the actin cytoskeleton that increases plasma membrane fluidity and decreases cell stiffness. Furthermore, we demonstrate that Cx43 interacts with the actin nucleator Arp2, the activity of which was shown to be necessary for Cx43-mediated actin rearrangement and lysosomal exocytosis following damage. These results define a novel mechanism of lysosomal quality control whereby Cx43-mediated actin remodelling potentiates the secretion of damaged lysosomes.

Indexed as

ActinsConnexin 43ExocytosisLysosomesAnimalsCell MembraneHumansMiceActinsConnexin 43Actin-remodellingArp2Connexin43ExocytosisLysosomal Damage

Identifiers

PMID39044100
PMCPMC11377567

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.