ArticleJournal of immunology (Baltimore, Md. : 1950)2018
Oxidant Signaling Mediated by Nox2 in Neutrophils Promotes Regenerative Myelopoiesis and Tissue Recovery following Ischemic Damage.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Myeloid DRP1 Sulfenylation Drives Reparative Macrophage Polarization and Neovascularization in Ischemic Muscle.Antioxidants (Basel, Switzerland) · 2026Article
- Integrating Bone-Brain Axis Modulation and Tea Consumption for Enhancing Neurovascular Resilience and Patient Rehabilitation Education.Food science & nutrition · 2026Review
- Diet-induced obesity induces oxidative stress and enhances H3K4me3 levels, driving nonresolving inflammation and myelopoiesis in hematopoietic stem and progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Myeloid DRP1 deficiency limits revascularization in ischemic muscles via inflammatory macrophage polarization and metabolic reprogramming.JCI insight · 2025Article
- Hematopoietic Stem Cells in Wound Healing Response.Advances in wound care · 2022Article
- Stem Cell Therapy for Sequestration of Traumatic Brain Injury-Induced Inflammation.International journal of molecular sciences · 2022Review
- Harnessing the anti-inflammatory properties of stem cells for transplant therapy in hemorrhagic stroke.Brain hemorrhages · 2020Article
- Macrophage Dysregulation and Impaired Skin Wound Healing in Diabetes.Frontiers in cell and developmental biology · 2020Review
- The phagocyte NOX2 NADPH oxidase in microbial killing and cell signaling.Current opinion in immunology · 2019Review
- Article
- Skin Wounding-Induced Monocyte Expansion in Mice Is Not Abrogated by IL-1 Receptor 1 Deficiency.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemic tissue damage activates hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM)-generating myeloid cells, and persistent HSPC activity may drive chronic inflammation and impair tissue recovery. Although increased reactive oxygen species in the BM regulate HSPC functions, their roles in myelopoiesis of activated HSPCs and subsequent tissue recovery during ischemic damage are not well understood. In this paper, we report that deletion of Nox2 NADPH oxidase in mice results in persistent elevations in BM HSPC activity and levels of inflammatory monocytes/macrophages in BM and ischemic tissue in a model of hindlimb ischemia. Ischemic tissue damage induces oxidants in BM such as elevations of hydrogen peroxide and oxidized phospholipids, which activate redox-sensitive Lyn kinase in a Nox2-dependent manner. Moreover, during tissue recovery after ischemic injury, this Nox2-ROS-Lyn kinase axis is induced by Nox2 in neutrophils that home to the BM, which inhibits HSPC activity and inflammatory monocyte generation and promotes tissue regeneration after ischemic damage. Thus, oxidant signaling in the BM mediated by Nox2 in neutrophils regulates myelopoiesis of HSPCs to promote regeneration of damaged tissue.
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Registered trials
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