Evidence map›Paper›PMID 18783175›Full record

ReviewAdvances in experimental medicine and biology2008

Mitochondrial oscillations in physiology and pathophysiology.

Miguel A Aon, Sonia Cortassa, Brian O'Rourke

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
22.9field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Adaptive behaviour and learning in slime moulds: the role of oscillations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

2 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

3 authors at 2 institutions in 1 country.

Miguel A AonDivision of Cardiology, Institute of Molecular Cardiobiology, The Johns Hopkins University Baltimore, Maryland, USA.
Sonia Cortassa
Brian O'Rourke
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

STRUCTURE OF MITOCHONDRIAL K+ CHANNELSP01HL081427 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI VAN EYK, JENNIFER E · 2005 to 2009
$11.2M
ENERGETIC REGULATION OF CARDIAC ION CHANNELSR37HL054598 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2005 to 2014
$3.7M
The Systems Biology of Sudden Cardiac DeathR33HL087338 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2007 to 2009
$949k
NHLBI NIH HHS P01 HL081427NHLBI NIH HHS R33 HL087338NHLBI NIH HHS R37 HL054598
6 · The paper itself

Abstract

Oscillations in chemical reactions and metabolic pathways have historically served as prototypes for understanding the dynamics of complex nonlinear systems. This chapter reviews the oscillatory behavior of mitochondria, with a focus on the mitochondrial oscillator dependent on reactive oxygen species (ROS), as first described in heart cells. Experimental and theoretical evidence now indicates that mitochondrial energetic variables oscillate autonomously as part of a network of coupled oscillators under both physiological and pathological conditions. The physiological domain is characterized by small-amplitude oscillations in mitochondrial membrane potential (delta psi(m)) showing correlated behavior over a wide range of frequencies, as determined using Power Spectral Analysis and Relative Dispersion Analysis of long term recordings of delta psi(m). Under metabolic stress, when the balance between ROS generation and ROS scavenging is perturbed, the mitochondrial network throughout the cell locks to one main low-frequency, high-amplitude oscillatory mode. This behavior has major pathological implications because the energy dissipation and cellular redox changes that occur during delta psi(m) depolarization result in suppression of electrical excitability and Ca2+ handling, the two main functions of the cardiac cell. In an ischemia/reperfusion scenario these alterations scale up to the level of the whole organ, giving rise to fatal arrhythmias.

Indexed as

AnimalsArrhythmias, CardiacBiological ClocksHumansIon ChannelsIon TransportMitochondriaMitochondria, HeartModels, BiologicalMyocytes, CardiacOxidative StressReactive Oxygen SpeciesIon ChannelsReactive Oxygen Species

Identifiers

PMID18783175
PMCPMC2692514
OpenAlexW181330873

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.