Evidence map›Paper›PMID 19285082›Full record

ReviewJournal of molecular and cellular cardiology2009

Cardioprotection by metabolic shut-down and gradual wake-up.

Lindsay S Burwell, Sergiy M Nadtochiy, Paul S Brookes

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 3 pooled it
7.9field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 3 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

28 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 1 institution in 1 country.

Lindsay S BurwellDepartment of Biochemistry and Biophysics, University of Rochester Medical Center, Rochester, NY 14642, USA.
Sergiy M Nadtochiy
Paul S Brookes
University of Rochester Medical Center · US

Funding

SIRT1, Nitro-Lipids and CardioprotectionR01HL071158 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S · 2003 to 2025
$7.7M
NHLBI NIH HHS R01 HL071158
6 · The paper itself

Abstract

Mitochondria play a critical role in cardiac function, and are also increasingly recognized as end effectors for various cardioprotective signaling pathways. Mitochondria use oxygen as a substrate, so by default their respiration is inhibited during hypoxia/ischemia. However, at reperfusion a surge of oxygen and metabolic substrates into the cell is thought to lead to rapid reestablishment of respiration, a burst of reactive oxygen species (ROS) generation and mitochondrial Ca(2+) overload. Subsequently these events precipitate opening of the mitochondrial permeability transition (PT) pore, which leads to myocardial cell death and dysfunction. Given that mitochondrial respiration is already inhibited during hypoxia/ischemia, it is somewhat surprising that many respiratory inhibitors can improve recovery from ischemia-reperfusion (IR) injury. In addition ischemic preconditioning (IPC), in which short non-lethal cycles of IR can protect against subsequent prolonged IR injury, is known to lead to endogenous inhibition of several respiratory complexes and glycolysis. This has led to a hypothesis that the wash-out of inhibitors or reversal of endogenous inhibition at reperfusion may afford protection by facilitating a more gradual wake-up of mitochondrial function, thereby avoiding a burst of ROS and Ca(2+) overload. This paper will review the evidence in support of this hypothesis, with a focus on inhibition of each of the mitochondrial respiratory complexes.

Indexed as

Electron Transport Complex IElectron Transport Complex IIElectron Transport Complex IIIElectron Transport Complex IVGlycolysisIschemic Preconditioning, MyocardialMitochondriaModels, BiologicalMyocardial Reperfusion InjuryNitric OxideElectron Transport Complex IElectron Transport Complex IIElectron Transport Complex IIIElectron Transport Complex IVNitric Oxide

Identifiers

PMID19285082
PMCPMC2683198
OpenAlexW2092708055

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.