Evidence map›Paper›PMID 16639504›Full record

ArticleJournal of human genetics2006

Humanin expression in skeletal muscles of patients with chronic progressive external ophthalmoplegia.

Tesseki Kin, Kazuma Sugie, Makito Hirano, Yu-Ichi Goto, Ichizo Nishino, Satoshi Ueno

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Humanin and diabetes mellitus: A review ofWorld journal of diabetes · 2022
    Review
  4. Review
  5. Article
  6. Mitochondrial-derived peptides in energy metabolism.American journal of physiology. Endocrinology and metabolism · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Functional Mitochondria in Health and Disease.Frontiers in endocrinology · 2017
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Humanin: a harbinger of mitochondrial-derived peptides?Trends in endocrinology and metabolism: TEM · 2013
    Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Tesseki KinDepartment of Neurology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan.
Kazuma SugieDepartment of Neurology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan.
Makito HiranoDepartment of Neurology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan. hirano_makito@yahoo.co.jp.
Yu-Ichi GotoDepartment of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Ichizo NishinoDepartment of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Satoshi UenoDepartment of Neurology, Nara Medical University School of Medicine, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan.
Nara Medical University · JPNational Center of Neurology and Psychiatry · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We showed that humanin (HN), an endogenous peptide against Alzheimer disease-related insults, was expressed in muscles of patients with chronic progressive external ophthalmoplegia (CPEO), a major mitochondrial disease. Because HN was recently found to block proapoptotic Bax function and exert its versatile cytoprotective effects in association with an increase in ATP levels, HN expression may thus reflect a physiological response against degenerative changes in the muscles of patients with CPEO. We found HN expression in all four patients examined, each of whom had different mitochondrial DNA mutations including two different single DNA deletions, multiple deletions, and no major mutations detected. We also found that HN expression was not linked to focal cytochrome c deficiency, strongly associated with the subtype of CPEO with single deletions. These results suggest that HN expression is more closely related to degenerative changes in all types of CPEO. Notably, HN was also expressed in non-degenerative muscle fibers of patients with CPEO or Leigh syndrome, who had the 8993T>G mutation in the mitochondrial ATPase 6 gene known to be associated with impaired ATP synthesis. Collectively, our findings suggest that HN may be specifically expressed in response to defects in energy production in muscles with mitochondrial abnormalities.

Indexed as

AdolescentChildChild, PreschoolCytochromes cDNA, MitochondrialFemaleGene ExpressionHumansInfantIntracellular Signaling Peptides and ProteinsLeigh DiseaseMaleMiddle AgedMitochondrial Proton-Translocating ATPasesMuscle, SkeletalOphthalmoplegia, Chronic Progressive ExternalCytochromes cDNA, MitochondrialF(6) ATPasehumaninIntracellular Signaling Peptides and ProteinsMitochondrial Proton-Translocating ATPasesOxidative Phosphorylation Coupling Factors

Identifiers

PMID16639504
OpenAlexW1984130379

What OpenQuestion holds

Textmetadata
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.