Stress erythropoiesis: definitions and models for its study.
Animals
Bone Morphogenetic Protein 4
/ genetics
Cellular Senescence
/ immunology
Cytokines
/ genetics
Erythrocytes
/ cytology
Erythroid Precursor Cells
/ cytology
Erythropoiesis
/ genetics
Gene Expression Regulation
Humans
Inflammation
Liver
/ cytology
Macrophages
/ cytology
Mice
Models, Biological
Phagocytosis
Spleen
/ cytology
Stress, Physiological
/ genetics
Journal
Experimental hematology
ISSN: 1873-2399
Titre abrégé: Exp Hematol
Pays: Netherlands
ID NLM: 0402313
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
24
04
2020
revised:
28
07
2020
accepted:
30
07
2020
pubmed:
5
8
2020
medline:
15
12
2020
entrez:
5
8
2020
Statut:
ppublish
Résumé
Steady-state erythropoiesis generates new erythrocytes at a constant rate, and it has enormous productive capacity. This production is balanced by the removal of senescent erythrocytes by macrophages in the spleen and liver. Erythroid homeostasis is highly regulated to maintain sufficient erythrocytes for efficient oxygen delivery to the tissues, while avoiding viscosity problems associated with overproduction. However, there are times when this constant production of erythrocytes is inhibited or is inadequate; at these times, erythroid output is increased to compensate for the loss of production. In some cases, increased steady-state erythropoiesis can offset the loss of erythrocytes but, in response to inflammation caused by infection or tissue damage, steady-state erythropoiesis is inhibited. To maintain homeostasis under these conditions, an alternative stress erythropoiesis pathway is activated. Emerging data suggest that the bone morphogenetic protein 4 (BMP4)-dependent stress erythropoiesis pathway is integrated into the inflammatory response and generates a bolus of new erythrocytes that maintain homeostasis until steady-state erythropoiesis can resume. In this perspective, we define the mechanisms that generate new erythrocytes when steady-state erythropoiesis is impaired and discuss experimental models to study human stress erythropoiesis.
Identifiants
pubmed: 32750404
pii: S0301-472X(20)30305-2
doi: 10.1016/j.exphem.2020.07.011
pmc: PMC7508762
mid: NIHMS1624452
pii:
doi:
Substances chimiques
BMP4 protein, human
0
Bone Morphogenetic Protein 4
0
Cytokines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
43-54.e2Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK080040
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK119865
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL146528
Pays : United States
Organisme : NIDDK NIH HHS
ID : R56 DK080040
Pays : United States
Informations de copyright
Copyright © 2020 ISEH -- Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
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