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Eryptosis in health and disease: A paradigm shift towards understanding the (patho)physiological implications of programmed cell death of erythrocytes
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
2017 (English)In: Blood reviews, ISSN 0268-960X, E-ISSN 1532-1681, Vol. 31, no 6, p. 349-361Article, review/survey (Refereed) Published
Abstract [en]

During the course of their natural ageing and upon injury, anucleate erythrocytes can undergo an unconventional apoptosis-like cell death, termed eryptosis. Eryptotic erythrocytes display a plethora of morphological alterations including volume reduction, membrane blebbing and breakdown of the membrane phospholipid asymmetry resulting in phosphatidylserine externalization which, in turn, mediates their phagocytic recognition and clearance from the circulation. Overall, the eryptosis machinery is tightly orchestrated by a wide array of endogenous mediators, ion channels, membrane receptors, and a host of intracellular signaling proteins. Enhanced eryptosis shortens the lifespan of circulating erythrocytes and confers a procoagulant phenotype; this phenomenon has been tangibly implicated in the pathogenesis of anemia, deranged microcirculation, and increased prothrombotic risk associated with a multitude of clinical conditions. Herein, we reviewed the molecular mechanisms dictating eryptosis and erythrophagocytosis and critically analyzed the current evidence leading to the pathophysiological ramifications of eryptotic cell death in the context of human disease.

Place, publisher, year, edition, pages
CHURCHILL LIVINGSTONE , 2017. Vol. 31, no 6, p. 349-361
Keywords [en]
Erythrocytes, Apoptosis, Eryptosis, Senescence, Erythirophagocytosis, Hemolysis, Anemia, Thrombosis, Deranged microcirculation
National Category
Hematology
Identifiers
URN: urn:nbn:se:umu:diva-142939DOI: 10.1016/j.blre.2017.06.001ISI: 000416204900001PubMedID: 28669393OAI: oai:DiVA.org:umu-142939DiVA, id: diva2:1165990
Available from: 2017-12-14 Created: 2017-12-14 Last updated: 2018-06-09Bibliographically approved

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Oldenborg, Per-Arne

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CiteExportLink to record
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  • apa
  • ieee
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