Evidence map›Paper›PMID 30917721›Full record

ArticleAutophagy2019

Mitochondrial respiratory chain deficiency inhibits lysosomal hydrolysis.

Lorena Fernandez-Mosquera, King Faisal Yambire, Renata Couto, Leonardo Pereyra, Kamil Pabis, Amy H Ponsford, Cátia V Diogo, Massimiliano Stagi, Ira Milosevic, Nuno Raimundo

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 165 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

36 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

10 authors at 3 institutions in 2 countries.

Lorena Fernandez-Mosqueraa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.ORCID 0000-0003-4606-5056
King Faisal Yambirea Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.ORCID 0000-0003-2417-450X
Renata Coutoa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.
Leonardo Pereyraa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.ORCID 0000-0002-9139-9664
Kamil Pabisa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.ORCID 0000-0002-1120-3079
Amy H Ponsfordf Institute of Translational Medicine, University of Liverpool , Liverpool , UK.
Cátia V Diogoa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.
Massimiliano Stagif Institute of Translational Medicine, University of Liverpool , Liverpool , UK.ORCID 0000-0002-5827-902X
Ira Milosevicd European Neuroscience Institute Goettingen, University Medical Center Goettingen and Max-Planck Society , Goettingen , Germany.ORCID 0000-0001-6440-3763
Nuno Raimundoa Institute of Cellular Biochemistry, University Medical Center Goettingen , Goettingen , Germany.ORCID 0000-0002-5988-9129
University of Göttingen · DEMax Planck Society · DEUniversity of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are key organelles for cellular metabolism, and regulate several processes including cell death and macroautophagy/autophagy. Here, we show that mitochondrial respiratory chain (RC) deficiency deactivates AMP-activated protein kinase (AMPK, a key regulator of energy homeostasis) signaling in tissue and in cultured cells. The deactivation of AMPK in RC-deficiency is due to increased expression of the AMPK-inhibiting protein FLCN (folliculin). AMPK is found to be necessary for basal lysosomal function, and AMPK deactivation in RC-deficiency inhibits lysosomal function by decreasing the activity of the lysosomal Ca

Indexed as

AMP-Activated Protein KinasesAnimalsAutophagosomesCalciumCell DeathElectron Transport Complex IFibroblastsHEK293 CellsHeLa CellsHumansLysosomesMiceMitochondriaMitochondrial DiseasesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesAMP-Activated Protein KinasesCalciumElectron Transport Complex IFLCN protein, humanMCOLN1 protein, humanphosphatidylinositol 3,5-diphosphatePhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPIKFYVE protein, humanProto-Oncogene ProteinsTransient Receptor Potential ChannelsTumor Suppressor ProteinsAMPKcalciumlysosomal CalysosomesMCOLN1mitochondriamitochondrial respiratory chain deficiency

Identifiers

PMID30917721
PMCPMC6693470
OpenAlexW2925694274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.