Evidence map›Paper›PMID 19377835›Full record

ReviewJournal of bioenergetics and biomembranes2009

Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue.

Shigeki Miyamoto, Anne N Murphy, Joan Heller Brown

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.6field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions ofInternational journal of molecular sciences · 2023
    Review
  7. Metabolic Inflexibility as a Pathogenic Basis for Atrial Fibrillation.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Mitochondrial Protection by PARP Inhibition.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. 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

3 authors at 1 institution in 1 country.

Shigeki MiyamotoDepartment of Pharmacology, University of California, 9500 Gilman Dr., La Jolla, San Diego, CA 92093-0636, USA. smiyamoto@ucsd.edu
Anne N Murphy
Joan Heller Brown
University of California, San Diego · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
RhoA mediated survival signals in cardiomyocytesR37HL028143 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER · 2010 to 2019
$4.0M
S1P, Rho and Akt signaling in cardiomyocyte survivalR01HL028143 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER · 1985 to 2009
$2.7M
NHLBI NIH HHS HL085577NHLBI NIH HHS HL28143NHLBI NIH HHS P01 HL085577NHLBI NIH HHS R01 HL028143NHLBI NIH HHS R37 HL028143
6 · The paper itself

Abstract

Cardiomyocyte death is now recognized as a critical factor in the development of heart disease. Mitochondria are not only responsible for energy production to ensure that cardiac output meets the body's energy demands, but they serve as critical integrators of cell survival signals. Numerous stressors are known to induce cell death by necrosis and/or apoptosis mediated through mitochondrial dysregulation. Anti- and pro-apoptotic Bcl-2 family proteins regulate apoptosis by controlling mitochondrial outer membrane permeability, whereas opening of the mitochondrial permeability transition pore (PT-pore) induces large amplitude permeability of the inner membrane and consequent rupture of the outer membrane. Akt is one of the best described survival kinases activated by receptor ligands and its activation preserves mitochondrial integrity and protects cardiomyocytes against necrotic and apoptotic death. The mechanisms responsible for Akt-mediated mitochondrial protection have not been fully elucidated. There is, however, accumulating evidence that multiple Akt target molecules, recruited through both transcriptional and post-transcriptional mechanisms, directly impinge upon and protect mitochondria. In this review we discuss mechanisms by which Akt activation can effect changes at the mitochondria that protect cardiomyocytes and attenuate pathophysiological responses of the heart.

Indexed as

ApoptosisAnimalsCell Membrane PermeabilityCell SurvivalEnzyme ActivationHumansMitochondria, HeartMitochondrial MembranesMyocardiumMyocytes, CardiacNecrosisOncogene Protein v-aktProto-Oncogene Proteins c-bcl-2Transcription, GeneticOncogene Protein v-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID19377835
PMCPMC2732429
OpenAlexW2163572624

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.