Research Topic

How Do Red Blood Cells Die?

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Despite decades of research, peaking in the late 1980’s, on the mechanisms of red blood cell (RBC) senescence and clearance (e.g., Magnani & De Flora (eds.) Red Blood Cell Aging, Plenum Press, 1991, a volume of 'Blood Cells' 14(1), 1988 - now 'Blood Cells, Molecules, and Diseases'), the issue remains ...

Despite decades of research, peaking in the late 1980’s, on the mechanisms of red blood cell (RBC) senescence and clearance (e.g., Magnani & De Flora (eds.) Red Blood Cell Aging, Plenum Press, 1991, a volume of 'Blood Cells' 14(1), 1988 - now 'Blood Cells, Molecules, and Diseases'), the issue remains open and controversial. Understanding of these mechanisms is an integral part of our progress in unraveling of the processes that control the RBC mass in patients with inappropriately high or low numbers of RBC. Without this knowledge we are unable to dissect the factors influencing RBC clearance under conditions of environmental hypoxia-reoxygenation or elucidate the causes of premature withdrawal of donor cells in the organism of the recipient.

Several hypotheses are currently dominating when clearance mechanisms are discussed. Among the markers of senescence that tag cells for clearance, loss of membrane surface and the concomitant increase in rigidity are named along with progressing oxidation. Further age-dependent changes resulting in clearance include hyper-phosphorylation of tyrosine residues within the cytosolic domain of band 3, leading to its aggregation, recognition of band 3 clusters by naturally occurring antibodies and opsonization. Moreover, dissipation of transmembrane Na+ gradients, loss of K+ and dehydration, Ca2+ overload, translocation of phosphatidylserine to the outer membrane leaflet, loss of CD47 from the cell membrane, are named as causes of clearance.

The resulting rheological and autoimmune theories of clearance, as well as eryptosis, necroptosis, neocytolysis and other theories describing RBC clearance do not peacefully co-exist, having own supporters and opponents forming camps and groups and rejecting each-others’ arguments. A Nomenclature Committee on Cell Death recently joined the fight, debating and criticizing the inappropriate use of the term “apoptosis/eryptosis” for qualifying as a “suicide” the death of RBCs.

We welcome all RBC researchers to submit manuscripts with their vision of the problem.

This Research Topic is supposed to be a forum to present arguments in favor or against one or the other processes that are believed to occur under physiologic, pathophysiologic and in vitro conditions or to come up with alternative views based on both existing reports and new experimental approaches. Particular questions that we suggest to address (but do not limit the authors to this short list of topics):
• What are the causes of RBC senescence and death?
• What are the markers of RBC senescence?
• What is a “dead red cell”?
• Do all RBCs die the same way or is there a probability for each cell to “die in bed” or end up “under the train”?
• Where do RBCs die? Are there differences in the process between spleen, liver, endothelium and others?
• What are the substantial differences between RBC-death in vivo and in vitro?
• What determines the proportions of "random" and "time-dependent" cell death of RBCs in various mammals?


Keywords: clearance, senescence, Ca2+, phospatidylserine, Band3, rheology, autoimmune response, eryptosis, necroptosis, neocytolysis, suicidal death, pathophysiology


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