ArticleNature communications2020
Chronic activation of endothelial MAPK disrupts hematopoiesis via NFKB dependent inflammatory stress reversible by SCGF.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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.
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Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
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- HO-1-modified umbilical cord MSCs alleviate pulmonary arterial hypertension by reducing inflammation and endothelial dysfunction.Stem cells translational medicine · 2026Article
- Cellular Signalling Networks in High Altitude Pulmonary Hypertension: From Canonical Pathways to Emerging Targets.Cell proliferation · 2026Review
- Myeloid PD-1 Regulates Astrocyte Development and Leads to Active Behaviours.Cell proliferation · 2026Article
- Multidimensional Evaluation of Lisdexamfetamine: Pharmacology, Therapeutic Use, Toxicity and Forensic Implications.Basic & clinical pharmacology & toxicology · 2025Review
- Effects of infliximab, an anti-TNF-α, on cyclophosphamide-induced bone marrow toxicity.Cancer chemotherapy and pharmacology · 2025Article
- Function of hematopoiesis and bone marrow niche in inflammation and non-hematopoietic diseases.Life medicine · 2025Review
- Atherosclerosis and Insulin Resistance: Is There a Link Between Them?Biomedicines · 2025Review
- Network pharmacology andWorld journal of gastroenterology · 2025Article
- The Interface of Gene Editing with Regenerative Medicine.Engineering (Beijing, China) · 2025Article
- Causal relationship between circulating inflammatory cytokines and the risk of hernia: a bidirectional Mendelian randomization study.The Journal of international medical research · 2025Article
- Suppression of thrombospondin-1-mediated inflammaging prolongs hematopoietic health span.Science immunology · 2025Article
- The aging hematopoietic stem cell niche: a mini review.Frontiers in hematology · 2025Article
- Exploring the Mechanism of Shen Qi Gui Oral Liquid against Chemotherapy- Induced Myelosuppression in Cancer Patients Based on Network Pharmacology and Molecular Docking.Combinatorial chemistry & high throughput screening · 2025Article
- Inflammation and DNA methylation in Alzheimer's disease: mechanisms of epigenetic remodelling by immune cell oxidants in the ageing brain.Redox report : communications in free radical research · 2024Review
- 27-Hydroxycholesterol Negatively Affects the Function of Bone Marrow Endothelial Cells in the Bone Marrow.International journal of molecular sciences · 2024Article
- [Inhibitory effect of 5-hydroxy-6,7-dimethoxyflavone on H1N1 influenza virus-induced ferroptosis and inflammation in A549 cells and its possible mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Inflammatory signals arising from the microenvironment have emerged as critical regulators of hematopoietic stem cell (HSC) function during diverse processes including embryonic development, infectious diseases, and myelosuppressive injuries caused by irradiation and chemotherapy. However, the contributions of cellular subsets within the microenvironment that elicit niche-driven inflammation remain poorly understood. Here, we identify endothelial cells as a crucial component in driving bone marrow (BM) inflammation and HSC dysfunction observed following myelosuppression. We demonstrate that sustained activation of endothelial MAPK causes NF-κB-dependent inflammatory stress response within the BM, leading to significant HSC dysfunction including loss of engraftment ability and a myeloid-biased output. These phenotypes are resolved upon inhibition of endothelial NF-κB signaling. We identify SCGF as a niche-derived factor that suppresses BM inflammation and enhances hematopoietic recovery following myelosuppression. Our findings demonstrate that chronic endothelial inflammation adversely impacts niche activity and HSC function which is reversible upon suppression of inflammation.
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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.