Evidence map›Paper›PMID 33528041›Full record

ArticleThe EMBO journal2021

Mitochondrial translation deficiency impairs NAD

Mikako Yagi, Takahiro Toshima, Rie Amamoto, Yura Do, Haruka Hirai, Daiki Setoyama, Dongchon Kang, Takeshi Uchiumi

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Spatial multiomics profiling reveals ZFP36-mediated immunometabolic reprogramming in bladder cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026
    Review
  7. Review
  8. MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

8 authors at 2 institutions in 1 country.

Mikako YagiDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Takahiro ToshimaDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Rie AmamotoDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Yura DoDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Haruka HiraiDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Daiki SetoyamaDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Dongchon KangDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.
Takeshi UchiumiDepartment of Clinical Chemistry and Laboratory Medicine, Kyushu University, Fukuoka, Japan.ORCID 0000-0002-3665-233X
Kyushu University · JPSeinan Jo Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial translation dysfunction is associated with neurodegenerative and cardiovascular diseases. Cells eliminate defective mitochondria by the lysosomal machinery via autophagy. The relationship between mitochondrial translation and lysosomal function is unknown. In this study, mitochondrial translation-deficient hearts from p32-knockout mice were found to exhibit enlarged lysosomes containing lipofuscin, suggesting impaired lysosome and autolysosome function. These mice also displayed autophagic abnormalities, such as p62 accumulation and LC3 localization around broken mitochondria. The expression of genes encoding for nicotinamide adenine dinucleotide (NAD

Indexed as

AnimalsCells, CulturedGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)Hypoxia-Inducible Factor 1, alpha SubunitLysosomesMiceMice, Inbred C57BLMicrotubule-Associated ProteinsMitochondria, HeartMitochondrial ProteinsNADNicotinamide-Nucleotide AdenylyltransferasePhosphoglycerate KinaseC1qbp protein, mouseGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMap1lc3b protein, mouseMicrotubule-Associated ProteinsMitochondrial ProteinsNADnicotinamide mononucleotide adenylyltransferase 3, mouseNicotinamide-Nucleotide AdenylyltransferasePgk1 protein, mousePhosphoglycerate KinaseGAPDHlysosomemitochondriaNAD+Nmnat3

Identifiers

PMID33528041
PMCPMC8047443
OpenAlexW3127283034

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.