Evidence map›Paper›PMID 21559063›Full record

ArticleFrontiers in physiology2011

Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury.

Amadou K S Camara, Martin Bienengraeber, David F Stowe

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2011. 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
5.2field-weighted citation impact, top 3% 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, 149 citations in OpenAlex.

  1. Review
  2. Mechanisms of Protection Against Oxidative Stress During Hibernation.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Differential CaFrontiers in synaptic neuroscience · 2025
    Article
  7. Article
  8. Complex II ambiguities-FADHThe Journal of biological chemistry · 2024
    Review
  9. Article
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  11. Review
  12. Review
  13. Review
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  15. Review
  16. Article
  17. Review
  18. Article
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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

3 authors at 2 institutions in 1 country.

Amadou K S CamaraDepartment of Anesthesiology, Medical College of Wisconsin Milwaukee, WI, USA.
Martin Bienengraeber
David F Stowe
Medical College of Wisconsin · USMarquette University · US

Funding

Stem Cell CoreP01GM066730 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI DASH, RANJAN K · 2003 to 2019
$23.6M
Cations and ROS in Modulating Mitochondrial Function in Normal and Ischemic HeartR01HL095122 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI CAMARA, AMADOU K., DASH, RANJAN K · 2010 to 2013
$2.1M
Mechanisms of photobiomodulation in myocardial reperfusion injuryR01HL098490 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI BIENENGRAEBER, MARTIN · 2010 to 2013
$1.5M
Mitochondrial Ca-sensitive K channel-induced superoxide and cardiac protectionR01HL089514 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STOWE, DAVID F · 2009 to 2012
$1.4M
NHLBI NIH HHS R01 HL089514NHLBI NIH HHS R01 HL095122NHLBI NIH HHS R01 HL098490NIGMS NIH HHS P01 GM066730
6 · The paper itself

Abstract

The mitochondrion is a vital component in cellular energy metabolism and intracellular signaling processes. Mitochondria are involved in a myriad of complex signaling cascades regulating cell death vs. survival. Importantly, mitochondrial dysfunction and the resulting oxidative and nitrosative stress are central in the pathogenesis of numerous human maladies including cardiovascular diseases, neurodegenerative diseases, diabetes, and retinal diseases, many of which are related. This review will examine the emerging understanding of the role of mitochondria in the etiology and progression of cardiovascular diseases and will explore potential therapeutic benefits of targeting the organelle in attenuating the disease process. Indeed, recent advances in mitochondrial biology have led to selective targeting of drugs designed to modulate or manipulate mitochondrial function, to the use of light therapy directed to the mitochondrial function, and to modification of the mitochondrial genome for potential therapeutic benefit. The approach to rationally treat mitochondrial dysfunction could lead to more effective interventions in cardiovascular diseases that to date have remained elusive. The central premise of this review is that if mitochondrial abnormalities contribute to the etiology of cardiovascular diseases (e.g., ischemic heart disease), alleviating the mitochondrial dysfunction will contribute to mitigating the severity or progression of the disease. To this end, this review will provide an overview of our current understanding of mitochondria function in cardiovascular diseases as well as the potential role for targeting mitochondria with potential drugs or other interventions that lead to protection against cell injury.

Indexed as

cardiac ischemia/reperfusioncardiac metabolismmitochondriamitochondrial Ca2+nitric oxideperoxynitritereactive oxygen speciestherapy

Identifiers

PMID21559063
PMCPMC3082167
OpenAlexW2160595902

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.