Evidence map›Paper›PMID 23806974›Full record

ArticleExperimental gerontology2013

Age-dependent mitochondrial energy dynamics in the mice heart: role of superoxide dismutase-2.

Kumuda C Das, Harish Muniyappa

Open access · hybridAbstract read
In one paragraph

Article in Experimental gerontology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  6. Modeling the human heart ex vivo-current possibilities and strive for future applications.Journal of tissue engineering and regenerative medicine · 2022
    Review
  7. Review
  8. Article
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  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. UPRCell research · 2018
    Review
  16. Article
  17. Mitophagy plays a central role in mitochondrial ageing.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Review
  18. Article
  19. Mitochondrial dysfunction in cardiac aging.Biochimica et biophysica acta · 2015
    Review
  20. Non-sirtuin histone deacetylases in the control of cardiac aging.Journal of molecular and cellular cardiology · 2015
    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

2 authors at 2 institutions in 1 country.

Kumuda C DasDepartment of Anesthesiology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. kumuda.das@ttuhsc.edu
Harish Muniyappa
Texas Tech University · USTexas Tech University Health Sciences Center · US

Funding

Endothelial dysfunction in aged Trx-deficient mice.R01HL107885 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI DAS, KUMUDA C · 2011 to 2014
$1.8M
Protective role of thioredoxin in endothelial apoptosis in the heart in ischemia-R01HL109397 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI DAS, KUMUDA C · 2011 to 2014
$1.5M
NHLBI NIH HHS 1R01HL109397-01NHLBI NIH HHS HL 1R01HL107885-01NHLBI NIH HHS R01 HL107885NHLBI NIH HHS R01 HL109397
6 · The paper itself

Abstract

The aging process alters cardiac physiology, decreases the number of cardiomyocytes and alters the energy metabolism. Mitochondrial dysfunction in aging is believed to cause these functional and phenotypic changes in the heart. Although precise understanding of alterations of mitochondrial respiration in aging is necessary to manage heart diseases in the elderly population conflicting data on the function of specific complex of electron transport chain of the heart mitochondria limits the intervention process. We have addressed these issues using the assay of mitochondrial coupling and electron flow to assess specific functional defects in mitochondria isolated from young or aged mice. Our results demonstrate that cardiac mitochondria from older mice utilize oxygen at a decreased rate via complex I, II or IV compared to younger mice. We further show that mitochondrial function decreases in young Sod2(+/-) mice heart compared to young wildtype mice. However, the mitochondrial function remains unchanged in older Sod2(+/-) mice heart compared to younger Sod2(+/-) mice heart. Further, the oxygen consumption remains similar in old wildtype mice and old Sod2(+/-) mice heart mitochondria. The expression and activity of Sod2 in young or old Sod2(+/-) mice heart remain unchanged. These data demonstrate that decreased oxygen utilization in older age could have resulted in decreased mitochondrial ROS-mediated oxidative damage requiring less Sod2 for protection against mitochondrial oxidative stress in older wildtype or older Sod2(+/-) mice.

Indexed as

AgingAnimalsCells, CulturedElectron TransportEndothelium, VascularHumansMiceMice, Inbred C57BLMice, KnockoutMitochondria, HeartOxygen ConsumptionRNA InterferenceSuperoxide DismutaseSuperoxide Dismutase 2Superoxide DismutaseSuperoxide Dismutase 2AgingBioenergeticsComplex IComplex IIElectron flowHeartMitochondriaMitochondrial couplingSODXF24

Identifiers

PMID23806974
PMCPMC4045457
OpenAlexW1997407309

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.