Evidence map›Paper›PMID 25172896›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Promoting PGC-1α-driven mitochondrial biogenesis is detrimental in pressure-overloaded mouse hearts.

Georgios Karamanlidis, Lorena Garcia-Menendez, Stephen C Kolwicz, Chi Fung Lee, Rong Tian

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Review
  7. Review
  8. Raising NADCirculation · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. The Role of Interventional Irisin on Heart Molecular Physiology.Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  13. PGC-1Frontiers in cell and developmental biology · 2022
    Review
  14. Review
  15. PERM1 regulates energy metabolism in the heartFrontiers in cardiovascular medicine · 2022
    Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Georgios KaramanlidisMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington.
Lorena Garcia-MenendezMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington.
Stephen C KolwiczMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington.
Chi Fung LeeMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington.
Rong TianMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington rongtian@u.washington.edu.
University of Washington · US

Funding

American Heart Association-American Stroke Association 13POST16200007
6 · The paper itself

Abstract

Mitochondrial dysfunction in animal models of heart failure is associated with downregulation of the peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α pathway. To test whether PGC-1α is an appropriate therapeutic target for increasing mitochondrial biogenesis and improving function in heart failure, we used a transgenic (TG) mouse model of moderate overexpression of PGC-1α (∼3-fold) in the heart. TG mice had small increases in citrate synthase activity and mitochondria size in the heart without alterations in myocardial energetics or cardiac function at baseline. In vivo dobutamine stress increased fractional shortening in wild-type mice, but this increase was attenuated in TG mice, whereas ex vivo isolated perfused TG hearts demonstrated normal functional and energetic response to high workload challenge. When subjected to pressure overload by transverse aortic constriction (TAC), TG mice displayed a significantly greater acute mortality for both male and female mice; however, long-term survival up to 8 wk was similar between the two groups. TG mice also showed a greater decrease in fractional shortening and a greater increase in left ventricular chamber dimension in response to TAC. Mitochondrial gene expression and citrate synthase activity were mildly increased in TG mice compared with wild-type mice, and this difference was also maintained after TAC. Our data suggest that a moderate level of PGC-1α overexpression in the heart compromises acute survival and does not improve cardiac function during chronic pressure overload in mice.

Indexed as

Mitochondrial TurnoverAnimalsCitrate (si)-SynthaseFemaleHeart FailureMaleMiceMitochondria, HeartMyocardial ContractionTranscription FactorsVentricular Dysfunction, LeftCitrate (si)-Synthaseperoxisome-proliferator-activated receptor-gamma coactivator-1Transcription Factorscardiac hypertrophyenergeticsheart failuremitochondrial biogenesisperoxisome proliferator-activated receptor-γ coactivator 1α

Identifiers

PMID25172896
PMCPMC4217009
OpenAlexW2048874320

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.