ArticleJournal of leukocyte biology2016
Perturbed MafB/GATA1 axis after burn trauma bares the potential mechanism for immune suppression and anemia of critical illness.
Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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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.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- GATA1 Transcriptionally Upregulates LMCD1, Promoting Ferroptosis in Sepsis-Associated Acute Kidney Injury Through the Hippo/YAP Pathway.The Kaohsiung journal of medical sciences · 2025Article
- Differential Response and Recovery Dynamics of HSPC Populations FollowingInternational journal of molecular sciences · 2025Article
- IL-1/MyD88-Dependent G-CSF and IL-6 Secretion Mediates Postburn Anemia.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- M-CSF supports medullary erythropoiesis and erythroid iron demand following burn injury through its activity on homeostatic iron recycling.Scientific reports · 2022Article
- The role of macrophages in thermal injury.International journal of burns and trauma · 2022Review
- The Presence of Nucleated Red Blood Cells as an Indicator for Increased Mortality and Morbidity in Burn Patients.Journal of burn care & research : official publication of the American Burn Association · 2021Article
- Transient Improvement in Erythropoiesis Is Achieved Via the Chaperone AHSP With Early Administration of Propranolol in Burn Patients.Journal of burn care & research : official publication of the American Burn Association · 2021Article
- Pediatric Burn Survivors Have Long-Term Immune Dysfunction With Diminished Vaccine Response.Frontiers in immunology · 2020Article
- A Shift in Myeloid Cell Phenotype via Down Regulation of Siglec-1 in Island Macrophages of Bone Marrow Is Associated With Decreased Late Erythroblasts Seen in Anemia of Critical Illness.Frontiers in medicine · 2019Article
- Deregulated iron metabolism in bone marrow from adenine-induced mouse model of chronic kidney disease.International journal of hematology · 2019Article
- Terminal Maturation of Orthochromatic Erythroblasts Is Impaired in Burn Patients.Journal of burn care & research : official publication of the American Burn Association · 2018Article
- Dysregulated myelopoiesis and hematopoietic function following acute physiologic insult.Current opinion in hematology · 2018Review
- Type I interferons drive inflammasome-independent emergency monocytopoiesis during endotoxemia.Scientific reports · 2017Article
- Thermal injury of the skin induces G-CSF-dependent attenuation of EPO-mediated STAT signaling and erythroid differentiation arrest in mice.Experimental hematology · 2017Article
- Discrete β-adrenergic mechanisms regulate early and late erythropoiesis in erythropoietin-resistant anemia.Surgery · 2017Article
- Myelo-erythroid commitment after burn injury is under β-adrenergic control via MafB regulation.American journal of physiology. Cell physiology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Patients who survive initial burn injury are susceptible to nosocomial infections. Anemia of critical illness is a compounding factor in burn patients that necessitates repeated transfusions, which further increase their susceptibility to infections and sepsis. Robust host response is dependent on an adequate number and function of monocytes/macrophages and dendritic cells. In addition to impaired RBC production, burn patients are prone to depletion of dendritic cells and an increase in deactivated monocytes. In steady-state hematopoiesis, RBCs, macrophages, and dendritic cells are all generated from a common myeloid progenitor within the bone marrow. We hypothesized in a mouse model of burn injury that an increase in myeloid-specific transcription factor V-maf musculoaponeurotic fibrosarcoma oncogene homolog B at the common myeloid progenitor stage steers their lineage potential away from the megakaryocyte erythrocyte progenitor production and drives the terminal fate of common myeloid progenitors to form macrophages vs. dendritic cells, with the consequences being anemia, monocytosis, and dendritic cell deficits. Results indicate that, even though burn injury stimulated bone marrow hematopoiesis by increasing multipotential stem cell production (Lin
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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 OpenQuestion graph.