ReviewCurrent topics in developmental biology2017
Regulation of Embryonic and Postnatal Development by the CSF-1 Receptor.
Review in Current topics in developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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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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Who cites it
75 citing papers in PubMed, 173 citations in OpenAlex.
- Review
- CSF1R regulates monocyte subset differentiation and intracellular metabolism.Nature communications · 2026Article
- Depletion and replacement of tissue-resident macrophages in mice with germ-line deletion of a conserved enhancer in the Csf1r locus.Development (Cambridge, England) · 2026Article
- Macrophages in embryonic development.Nature reviews. Immunology · 2026Review
- Identification of chromosomal abnormalities in miscarriages using single-nucleotide polymorphism arrays.Archives of gynecology and obstetrics · 2026Article
- Expression and Role of Colony Stimulating Factor 1 Receptor During Odontogenesis.Journal of developmental biology · 2026Article
- A strategy of microglia replacement alleviates microgliopathy in a CSF1R I794T hotspot mutation mouse model of CSF1R-related disorder.Cell reports. Medicine · 2026Article
- Microglial colonization of the developing mouse brain is controlled by both microglial and neural CSF-1.The EMBO journal · 2026Article
- Controlled Delivery of a Neurotrophic Factor in the Adult Mouse Brain Using Engineered Microglia.bioRxiv : the preprint server for biology · 2025Article
- Mutation in the rat interleukin 34 gene impacts macrophage development, homeostasis, and inflammation.Life science alliance · 2025Article
- WNK1 mediates M-CSF-induced macropinocytosis to enforce macrophage lineage fidelity.Nature communications · 2025Article
- Microglial depletion prevents visual deficits and retinal ganglion cell loss induced by early life stress in adult animals.Scientific reports · 2025Article
- Typical development of synaptic and neuronal properties can proceed without microglia in the cortex and thalamus.Nature neuroscience · 2025Article
- Interleukin-34 orchestrates bone formation through its binding to bone morphogenic proteins.Theranostics · 2025Article
- Wild-type bone marrow cells repopulate tissue resident macrophages and reverse the impacts of homozygous CSF1R mutation.PLoS genetics · 2025Article
- Physiological roles of embryonic microglia and their perturbation by maternal inflammation.Frontiers in cellular neuroscience · 2025Review
- Switch to phagocytic microglia by CSFR1 inhibition drives amyloid-beta clearance from glutamatergic terminals rescuing LTP in acute hippocampal slices.Translational psychiatry · 2024Article
- Identification and characterization of a novel intronic splicing mutation in CSF1R-related leukoencephalopathy.CNS neuroscience & therapeutics · 2024Article
- CSF1R antagonism results in increased supraspinal infiltration in EAE.Journal of neuroinflammation · 2024Article
- The ubiquitin ligases Cbl and Cbl-b regulate macrophage growth by controlling CSF-1R import into macropinosomes.Molecular biology of the cell · 2024Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages are found in all tissues and regulate tissue morphogenesis during development through trophic and scavenger functions. The colony stimulating factor-1 (CSF-1) receptor (CSF-1R) is the major regulator of tissue macrophage development and maintenance. In combination with receptor activator of nuclear factor κB (RANK), the CSF-1R also regulates the differentiation of the bone-resorbing osteoclast and controls bone remodeling during embryonic and early postnatal development. CSF-1R-regulated macrophages play trophic and remodeling roles in development. Outside the mononuclear phagocytic system, the CSF-1R directly regulates neuronal survival and differentiation, the development of intestinal Paneth cells and of preimplantation embryos, as well as trophoblast innate immune function. Consistent with the pleiotropic roles of the receptor during development, CSF-1R deficiency in most mouse strains causes embryonic or perinatal death and the surviving mice exhibit multiple developmental and functional deficits. The CSF-1R is activated by two dimeric glycoprotein ligands, CSF-1, and interleukin-34 (IL-34). Homozygous Csf1-null mutations phenocopy most of the deficits of Csf1r-null mice. In contrast, Il34-null mice have no gross phenotype, except for decreased numbers of Langerhans cells and microglia, indicating that CSF-1 plays the major developmental role. Homozygous inactivating mutations of the Csf1r or its ligands have not been reported in man. However, heterozygous inactivating mutations in the Csf1r lead to a dominantly inherited adult-onset progressive dementia, highlighting the importance of CSF-1R signaling in the brain.
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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.