ArticleBlood2016
The macrophage contribution to stress erythropoiesis: when less is enough.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed.
- Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025Review
- Extramedullary hematopoiesis in cancer.Experimental & molecular medicine · 2024Review
- Homeostatic Functions of Tissue-Resident Macrophages and Their Role in Tissue Maintenance.Results and problems in cell differentiation · 2024Review
- Kindlin-3 deficiency leads to impaired erythropoiesis and erythrocyte cytoskeleton.Blood advances · 2023Article
- Article
- Targeting Stress Erythropoiesis Pathways in Cancer.Frontiers in physiology · 2022Review
- The Multiple Facets of Iron Recycling.Genes · 2021Review
- PPARγ is essential for the development of bone marrow erythroblastic island macrophages and splenic red pulp macrophages.The Journal of experimental medicine · 2021Article
- Combined liver-cytokine humanization comes to the rescue of circulating human red blood cells.Science (New York, N.Y.) · 2021Article
- Article
- Transcriptional Control of Gene Expression and the Heterogeneous Cellular Identity of Erythroblastic Island Macrophages.Frontiers in genetics · 2021Review
- The mechanisms of pathological extramedullary hematopoiesis in diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Nrf2 deficiency in mice attenuates erythropoietic stress-related macrophage hypercellularity.Experimental hematology · 2020Article
- Reappraising the role of α5 integrin and the microenvironmental support in stress erythropoiesis.Experimental hematology · 2020Article
- Article
- Monocyte-derived macrophages expand the murine stress erythropoietic niche during the recovery from anemia.Blood · 2018Article
- Article
- Glucocorticoids induce differentiation of monocytes towards macrophages that share functional and phenotypical aspects with erythroblastic island macrophages.Haematologica · 2018Article
- The Shape Shifting Story of Reticulocyte Maturation.Frontiers in physiology · 2018Review
- Interaction of the Macrophage and Primitive Erythroid Lineages in the Mammalian Embryo.Frontiers in immunology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Although the importance of native bone marrow and spleen macrophages in enhancing baseline and stress erythropoiesis has been emphasized over several decades, their kinetic and phenotypic changes during a variety of stress responses have been unclear. Furthermore, whether monocyte-derived recruited macrophages can functionally substitute for inadequate or functionally impaired native macrophages has been controversial and seem to be not only tissue- but also stress-type dependent. To provide further insight into these issues, we made detailed observations at baseline and post-erythroid stress (E-stress) in 2 mouse models with genetically depressed macrophage numbers and compared them to their controls. We documented that, irrespective of the stress-induced (hemolytic or post-erythropoietin [Epo]) treatment, only native CD11b(lo) splenic macrophages expand dramatically post-stress in normal mice without significant changes in the monocyte-derived CD11b(hi) subset. The latter remained a minority and did not change post-stress in 2 genetic models lacking either Spi-C or VCAM-1 with impaired native macrophage proliferative expansion. Although CD11b(lo) macrophages in these mice were one-fifth of normal at their peak response, surprisingly, their erythroid response was not compromised and was similar to controls. Thus, despite the prior emphasis on numerical macrophage reliance to provide functional rescue from E-stress, our data highlight the importance of previously described non-macrophage-dependent pathways activated under certain stress conditions to compensate for low macrophage numbers.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.