Evidence map›Paper›PMID 22878108›Full record

ReviewInternational review of cell and molecular biology2012

Cell biology of ischemia/reperfusion injury.

Theodore Kalogeris, Christopher P Baines, Maike Krenz, Ronald J Korthuis

Open access · greenAbstract readReview
In one paragraph

Review in International review of cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,079 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,079citing papers in PubMed, 1 pooled it
168.0field-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

1,079 citing papers in PubMed, 1 synthesis or guideline pooled it, 2,106 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Curcumin in ischemia-reperfusion injury across multiple organs: A review.The Journal of international medical research · 2026
    Review
  19. Article
  20. Article

1,019 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

4 authors at 1 institution in 1 country.

Theodore KalogerisDepartment of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, USA.
Christopher P Baines
Maike Krenz
Ronald J Korthuis
University of Missouri · US

Funding

Regulation Microvascular: Smooth Muscle Contraction ECM-Integrin-CytoskeletalP01HL095486 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DAVIS, GEORGE E · 2010 to 2014
$8.4M
Molecular Identity of the Cardiac Mitochondrial PoreR01HL094404 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BAINES, CHRISTOPHER P · 2009 to 2018
$3.6M
Ethanol Prevents Microvascular DysfunctionR01AA014945 · NIAAA · UNIVERSITY OF MISSOURI-COLUMBIA · PI KORTHUIS, RONALD JOHN · 2006 to 2010
$1.6M
Identifying novel components of the cardiac necrotic programR21HL092327 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BAINES, CHRISTOPHER P · 2008 to 2009
$412k
NHLBI NIH HHS HL092327NHLBI NIH HHS HL094404NHLBI NIH HHS HL-095486NHLBI NIH HHS P01 HL095486NHLBI NIH HHS R01 HL094404NHLBI NIH HHS R21 HL092327NIAAA NIH HHS AA-014945NIAAA NIH HHS R01 AA014945
6 · The paper itself

Abstract

Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues.

Indexed as

AnimalsCell BiologyCell DeathFetusHumansModels, BiologicalReperfusion InjuryRisk Factors

Identifiers

PMID22878108
PMCPMC3904795
OpenAlexW204998232

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.