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Cited by 718

The DOI matches its Crossref record; 869 of the 869 references it cites were found in a registry or an index.

Ischemia/Reperfusion

Open access
Kalogeris, Theodore, Baines, Christopher P., Krenz, Maike, Korthuis, Ronald J.·2016·Comprehensive Physiology
DOI 10.1002/cphy.c160006
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Abstract

Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease. © 2017 American Physiological Society. Compr Physiol 7:113-170, 2017.

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Citations

Cites

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Metadata

Authors
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J.
Venue
Comprehensive Physiology
Publisher
Wiley
Published
2016-12-06
Volume
7
Issue
1
Pages
113-170
ISSN
2040-4603 (ISSN-L)
DOI
10.1002/cphy.c160006
OpenAlex
W4211073154
Cited by
718
References
869
Type
other
Language
en
Open access
green

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