Evidence map›Paper›PMID 26191650›Full record

ReviewBiochimica et biophysica acta2015

Mitochondrial dysfunction in cardiac aging.

Autumn Tocchi, Ellen K Quarles, Nathan Basisty, Lemuel Gitari, Peter S Rabinovitch

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 146 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Role of Mitochondrial Dynamics in Skin Homeostasis: An Update.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

9 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

5 authors at 1 institution in 1 country.

Autumn TocchiUniversity of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: uw.tocchi@gmail.com.
Ellen K QuarlesUniversity of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: equarles@gmail.com.
Nathan BasistyUniversity of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: nbasisty@uw.edu.
Lemuel GitariUniversity of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: mlemuel@uw.edu.
Peter S RabinovitchUniversity of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA. Electronic address: petersr@u.washington.edu.
University of Washington · US

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI PRUSKY, GLEN THOMAS · 1985 to 2021
$29.6M
GENETIC APPROACHES TO AGING RESEARCHT32AG000057 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 1985 to 2019
$14.2M
The importance of mTOR signaling in cardiac aging and lifespan in mammalsR01AG038550 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 2010 to 2014
$1.5M
NIA NIH HHS P01 AG001751NIA NIH HHS R01 AG038550NIA NIH HHS T32 AG000057
6 · The paper itself

Abstract

Cardiovascular diseases are the leading cause of death in most developed nations. While it has received the least public attention, aging is the dominant risk factor for developing cardiovascular diseases, as the prevalence of cardiovascular diseases increases dramatically with increasing age. Cardiac aging is an intrinsic process that results in impaired cardiac function, along with cellular and molecular changes. Mitochondria play a great role in these processes, as cardiac function is an energetically demanding process. In this review, we examine mitochondrial dysfunction in cardiac aging. Recent research has demonstrated that mitochondrial dysfunction can disrupt morphology, signaling pathways, and protein interactions; conversely, mitochondrial homeostasis is maintained by mechanisms that include fission/fusion, autophagy, and unfolded protein responses. Finally, we describe some of the recent findings in mitochondrial targeted treatments to help meet the challenges of mitochondrial dysfunction in aging.

Indexed as

AgingAnimalsAutophagyCaloric RestrictionCardiolipinsDNA DamageEnergy MetabolismHeartHomeostasisHumansMitochondriaProteinsSignal TransductionUnfolded Protein ResponseCardiolipinsProteinsAgingHeartMitochondrial dysfunctionMitostasis

Identifiers

PMID26191650
PMCPMC4575872
OpenAlexW1191391069

What OpenQuestion holds

Textmetadata
LicenceTDM
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.