Journal
CELLS
Volume 9, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/cells9030634
Keywords
stress erythropoiesis; erythroblastic islands; pro-inflammatory cytokines; erythrophagocytosis; anemia of inflammation
Categories
Funding
- National Institutes of Health [RO1 DK080040, RO1 DK119865, RO1 HL146528]
- USDA-NIFA Hatch Project [PEN04605, 1010021]
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Bone marrow medullary erythropoiesis is primarily homeostatic. It produces new erythrocytes at a constant rate, which is balanced by the turnover of senescent erythrocytes by macrophages in the spleen. Despite the enormous capacity of the bone marrow to produce erythrocytes, there are times when it is unable to keep pace with erythroid demand. At these times stress erythropoiesis predominates. Stress erythropoiesis generates a large bolus of new erythrocytes to maintain homeostasis until steady state erythropoiesis can resume. In this review, we outline the mechanistic differences between stress erythropoiesis and steady state erythropoiesis and show that their responses to inflammation are complementary. We propose a new hypothesis that stress erythropoiesis is induced by inflammation and plays a key role in maintaining erythroid homeostasis during inflammatory responses.
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