Evidence map›Paper›PMID 21964191›Full record

ReviewJournal of molecular and cellular cardiology2012

Measuring mitochondrial function in intact cardiac myocytes.

Elena N Dedkova, Lothar A Blatter

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing 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

72 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Guidelines for mitochondrial RNA analysis.Molecular therapy. Nucleic acids · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Pore-like diffusion barriers in murine cardiac myocytes.bioRxiv : the preprint server for biology · 2023
    Article
  18. Review
  19. Article
  20. Review

12 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

2 authors at 1 institution in 1 country.

Elena N DedkovaDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL 60612, USA.
Lothar A Blatter
Rush University Medical Center · US

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
E/C COUPLING AND CALCIUM REGULATION IN ATRIAL MYOCYTESR01HL062231 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI BLATTER, LOTHAR A · 1999 to 2012
$4.4M
MItochondrial Dysfunction in Cardiac Hypertrophy and FailureR01HL101235 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BERS, DONALD M, BLATTER, LOTHAR A · 2010 to 2013
$2.8M
NHLBI NIH HHS HL101235NHLBI NIH HHS HL62231NHLBI NIH HHS HL80101NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL062231NHLBI NIH HHS R01 HL101235
6 · The paper itself

Abstract

Mitochondria are involved in cellular functions that go beyond the traditional role of these organelles as the power plants of the cell. Mitochondria have been implicated in several human diseases, including cardiac dysfunction, and play a role in the aging process. Many aspects of our knowledge of mitochondria stem from studies performed on the isolated organelle. Their relative inaccessibility imposes experimental difficulties to study mitochondria in their natural environment-the cytosol of intact cells-and has hampered a comprehensive understanding of the plethora of mitochondrial functions. Here we review currently available methods to study mitochondrial function in intact cardiomyocytes. These methods primarily use different flavors of fluorescent dyes and genetically encoded fluorescent proteins in conjunction with high-resolution imaging techniques. We review methods to study mitochondrial morphology, mitochondrial membrane potential, Ca(2+) and Na(+) signaling, mitochondrial pH regulation, redox state and ROS production, NO signaling, oxygen consumption, ATP generation and the activity of the mitochondrial permeability transition pore. Where appropriate we complement this review on intact myocytes with seminal studies that were performed on isolated mitochondria, permeabilized cells, and in whole hearts.

Indexed as

Adenosine TriphosphateAnimalsCalciumCalcium SignalingHumansHydrogen-Ion ConcentrationIntracellular MembranesMembrane Potential, MitochondrialMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocytes, CardiacNitric OxideOxidation-ReductionOxygen ConsumptionPermeabilityAdenosine TriphosphateCalciumMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNitric OxideReactive Oxygen SpeciesSodium

Identifiers

PMID21964191
PMCPMC3246130
OpenAlexW1983492852

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.