An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice.
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Cord Sunderkötter | K. Scharffetter-Kochanek | C. Sunderkötter | M. Wlaschek | J. Weiss | Karin Scharffetter-Kochanek | Meinhard Wlaschek | T. Peters | Stefan Wieschalka | Thorsten Peters | Anca Sindrilaru | Adelheid Hainzl | Corina Baican | Adrian Baican | Henriette Peter | Susanne Schatz | Yu Qi | Andrea Schlecht | Johannes M Weiss | A. Sindrilaru | A. Baican | A. Hainzl | Yu Qi | S. Schatz | H. Peter | C. Baican | S. Wieschalka | A. Schlecht
[1] Werner Müller,et al. Differential Roles of Macrophages in Diverse Phases of Skin Repair , 2010, The Journal of Immunology.
[2] M. Salmon,et al. A stromal address code defined by fibroblasts. , 2005, Trends in immunology.
[3] G. Barbarini,et al. Primary Pulmonary Hypertension in HIV Patients: A Systematic Review , 2001, Angiology.
[4] S. Hanauer,et al. For Personal Use. Only Reproduce with Permission from the Lancet Publishing Group , 2022 .
[5] M. Robson,et al. Wound Infection: A Failure of Wound Healing Caused by an Imbalance of Bacteria , 1997 .
[6] Silvano Sozzani,et al. The chemokine system in diverse forms of macrophage activation and polarization. , 2004, Trends in immunology.
[7] J. Sedivy,et al. Cellular Senescence in Aging Primates , 2006, Science.
[8] P. Libby,et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions , 2007, The Journal of experimental medicine.
[9] T. Krieg,et al. Expression and proteolysis of vascular endothelial growth factor is increased in chronic wounds. , 2000, The Journal of investigative dermatology.
[10] H. Niederegger,et al. Autocrine formation of hepcidin induces iron retention in human monocytes. , 2008, Blood.
[11] R N Maini,et al. Infliximab and methotrexate in the treatment of rheumatoid arthritis. Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group. , 2000, The New England journal of medicine.
[12] S. Gordon. Alternative activation of macrophages , 2003, Nature Reviews Immunology.
[13] A. Salim. The role of oxygen-derived free radicals in the management of venous (varicose) ulceration: A new approach , 1991, World journal of surgery.
[14] H. Zeidler,et al. Treatment of active ankylosing spondylitis with infliximab: a randomised controlled multicentre trial , 2002, The Lancet.
[15] M. Streit,et al. Topical application of the tumour necrosis factor‐α antibody infliximab improves healing of chronic wounds , 2006, International wound journal.
[16] N. Rooijen,et al. Depletion and repopulation of macrophages in spleen and liver of rat after intravenous treatment with liposome-encapsulated dichloromethylene diphosphonate , 1990, Cell and Tissue Research.
[17] G M Lyons,et al. Haemodynamic study examining the response of venous blood flow to electrical stimulation of the gastrocnemius muscle in patients with chronic venous disease. , 2006, European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery.
[18] Z. Ackerman,et al. Overload of iron in the skin of patients with varicose ulcers. Possible contributing role of iron accumulation in progression of the disease. , 1988, Archives of dermatology.
[19] bc David J. Margolisa,et al. Venous leg ulcer: incidence and prevalence in the elderly. , 2002, Journal of the American Academy of Dermatology.
[20] Wei Li,et al. The iron hypothesis of atherosclerosis and its clinical impact , 2003, Annals of medicine.
[21] M. Davies,et al. Direct Detection and Quantification of Transition Metal Ions in Human Atherosclerotic Plaques: Evidence for the Presence of Elevated Levels of Iron and Copper , 2004, Arteriosclerosis, thrombosis, and vascular biology.
[22] F. Gottrup,et al. Immunohistochemical characterization of the cutaneous cellular infiltrate in different areas of chronic leg ulcers , 1995, APMIS : acta pathologica, microbiologica, et immunologica Scandinavica.
[23] K. Krogfelt,et al. Why chronic wounds will not heal: a novel hypothesis , 2008, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[24] N. Carter,et al. A DNA damage checkpoint response in telomere-initiated senescence , 2003, Nature.
[25] S. Goerdt,et al. Other functions, other genes: alternative activation of antigen-presenting cells. , 1999, Immunity.
[26] G. Moneta,et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. , 2004, Journal of vascular surgery.
[27] Emmanuel A Theodorakis,et al. Anti-TNF-alpha therapies: the next generation. , 2003, Nature reviews. Drug discovery.
[28] D. Kipling,et al. Fibroblast dysfunction is a key factor in the non-healing of chronic venous leg ulcers. , 2008, The Journal of investigative dermatology.
[29] J. Gerber,et al. Reversing lipopolysaccharide toxicity by ligating the macrophage Fc gamma receptors. , 2001, Journal of immunology.
[30] Alberto Mantovani,et al. Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression1 , 2006, The Journal of Immunology.
[31] B. Halliwell,et al. Iron, Atherosclerosis, and Neurodegeneration: A Key Role for Cholesterol in Promoting Iron‐Dependent Oxidative Damage? , 2004, Annals of the New York Academy of Sciences.
[32] S. Tognazzo,et al. Hemochromatosis C282Y gene mutation increases the risk of venous leg ulceration. , 2005, Journal of vascular surgery.
[33] G. Weiss,et al. Cytokine Mediated Regulation of Iron Transport in Human Monocytic Cells , 2003 .
[34] A. Lackner,et al. CD163, a marker of perivascular macrophages, is up-regulated by microglia in simian immunodeficiency virus encephalitis after haptoglobin-hemoglobin complex stimulation and is suggestive of breakdown of the blood-brain barrier. , 2008, The American journal of pathology.
[35] T. Breit,et al. Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity , 2009, Nature Cell Biology.
[36] S. Tognazzo,et al. The overlapping of local iron overload and HFE mutation in venous leg ulcer pathogenesis. , 2006, Free radical biology & medicine.
[37] R. Ross,et al. The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum. , 1975, The American journal of pathology.
[38] N. Sharpless,et al. Ink4a/Arf expression is a biomarker of aging. , 2004, The Journal of clinical investigation.
[39] E. Zandi,et al. Signaling Role of Intracellular Iron in NF-κB Activation* , 2003, The Journal of Biological Chemistry.
[40] L. Zacharski,et al. Hereditary haemochromatosis and the hypothesis that iron depletion protects against ischemic heart disease , 2001, European journal of clinical investigation.
[41] F. F. F. F. Aws S. Salim Ph.D.. The role of oxygen-derived free radicals in the management of venous (varicose) ulceration: A new approach , 2005, World Journal of Surgery.
[42] Jerry Kaplan,et al. Regulation of iron acquisition and storage: consequences for iron-linked disorders , 2008, Nature Reviews Molecular Cell Biology.
[43] Jiri Bartek,et al. p16INK4A is a robust in vivo biomarker of cellular aging in human skin , 2006, Aging cell.
[44] B. Hinz,et al. Wound‐healing defect of CD18−/− mice due to a decrease in TGF‐β1 and myofibroblast differentiation , 2005, The EMBO journal.
[45] T. Kepler,et al. The T helper type 2 response to cysteine proteases requires dendritic cell–basophil cooperation via ROS-mediated signaling , 2010, Nature Immunology.
[46] K. Scharffetter-Kochanek,et al. Oxidative stress in chronic venous leg ulcers , 2005, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[47] A. Singer,et al. Cutaneous wound healing. , 1999, The New England journal of medicine.
[48] S. Raju,et al. Clinical practice. Chronic venous insufficiency and varicose veins. , 2009, The New England journal of medicine.
[49] R. Diegelmann,et al. Ability of chronic wound fluids to degrade peptide growth factors is associated with increased levels of elastase activity and diminished levels of proteinase inhibitors , 1997, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[50] M. Maves,et al. Deferoxamine Decreases Necrosis in Dorsally Based Pig Skin Flaps , 1989, Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery.
[51] Lyle L. Moldawer,et al. Anti-TNF-α therapies: the next generation , 2003, Nature Reviews Drug Discovery.
[52] V. Nizet,et al. TLR4-dependent hepcidin expression by myeloid cells in response to bacterial pathogens. , 2006, Blood.
[53] H. Tsukamoto,et al. Iron Causes Interactions of TAK1, p21ras, and Phosphatidylinositol 3-Kinase in Caveolae to Activate IκB Kinase in Hepatic Macrophages* , 2007, Journal of Biological Chemistry.
[54] Csaba Szabó,et al. Peroxynitrite: biochemistry, pathophysiology and development of therapeutics , 2007, Nature Reviews Drug Discovery.
[55] M. Stacey,et al. Iron and 8-isoprostane levels in acute and chronic wounds. , 2003, The Journal of investigative dermatology.
[56] P. Smith. Update on chronic-venous-insufficiency-induced inflammatory processes. , 2001, Angiology.
[57] J. Duffield. The inflammatory macrophage , 2003 .
[58] R. Cooper,et al. Use of topical corticosteroids on chronic leg ulcers. , 2007, Journal of wound care.
[59] N. Van Rooijen,et al. Activated macrophages are essential in a murine model for T cell-mediated chronic psoriasiform skin inflammation. , 2006, The Journal of clinical investigation.
[60] W. Liles,et al. The phagocytes: neutrophils and monocytes. , 2008, Blood.
[61] P. Zamboni. The Big Idea: Iron-Dependent Inflammation in Venous Disease and Proposed Parallels in Multiple Sclerosis , 2006, Journal of the Royal Society of Medicine.
[62] J. Gerber,et al. Reversing Lipopolysaccharide Toxicity by Ligating the Macrophage Fcγ Receptors1 , 2001, The Journal of Immunology.
[63] S. Sato,et al. Delayed wound healing in the absence of intercellular adhesion molecule-1 or L-selectin expression. , 2000, The American journal of pathology.
[64] J. Duffield. The inflammatory macrophage: a story of Jekyll and Hyde. , 2003, Clinical science.
[65] M. Robson. Wound Infection: A Failure of Wound Healing Caused by an Imbalance of Bacteria , 1997 .
[66] K. Scharffetter-Kochanek,et al. Protease inhibitors protect growth factor activity in chronic wounds , 1997, The British journal of dermatology.
[67] J. Dormandy,et al. Causes of venous ulceration: a new hypothesis , 1988 .
[68] G. Schmid-Schönbein,et al. Leukocyte activation in patients with venous insufficiency. , 1999, Journal of vascular surgery.
[69] D. Margolis,et al. Venous leg ulcer: incidence and prevalence in the elderly. , 2002, Journal of the American Academy of Dermatology.
[70] F. Grinnell,et al. Wound fluid from chronic leg ulcers contains elevated levels of metalloproteinases MMP-2 and MMP-9. , 1993, The Journal of investigative dermatology.
[71] B. Walzog,et al. Wound healing defect of Vav3-/- mice due to impaired {beta}2-integrin-dependent macrophage phagocytosis of apoptotic neutrophils. , 2009, Blood.
[72] Paul Martin,et al. Wound Healing--Aiming for Perfect Skin Regeneration , 1997, Science.
[73] J. Edwards,et al. Exploring the full spectrum of macrophage activation , 2008, Nature Reviews Immunology.
[74] M. Gotsman,et al. Deferoxamine improves left ventricular function in beta-thalassemia. , 1986, Archives of internal medicine.
[75] G. Dow,et al. Infection in chronic wounds: controversies in diagnosis and treatment. , 1999, Ostomy/wound management.
[76] K. Scharffetter-Kochanek,et al. Selective pick-up of increased iron by deferoxamine-coupled cellulose abrogates the iron-driven induction of matrix-degrading metalloproteinase 1 and lipid peroxidation in human dermal fibroblasts in vitro: a new dressing concept. , 2001, The Journal of investigative dermatology.
[77] J. O’Shea,et al. Cytokine signaling modules in inflammatory responses. , 2008, Immunity.
[78] J. Menzoian,et al. Fibroblasts cultured from venous ulcers display cellular characteristics of senescence. , 1998, Journal of vascular surgery.
[79] W. Eaglstein,et al. Causes and effects of the chronic inflammation in venous leg ulcers. , 2000, Acta dermato-venereologica. Supplementum.
[80] G. Riethmüller,et al. Synergistic effect of tumor necrosis factor-? and interferon-? on collagen synthesis of human skin fibroblasts , 1989 .
[81] Topical application of the tumour necrosis factor‐a antibody infliximab improves healing of chronic wounds , 2006 .
[82] K. Harding,et al. Non-healing is associated with persistent stimulation of the innate immune response in chronic venous leg ulcers. , 2010, Journal of dermatological science.
[83] G. Riethmüller,et al. Synergistic effect of tumor necrosis factor-alpha and interferon-gamma on collagen synthesis of human skin fibroblasts in vitro. , 1989, Experimental Cell Research.
[84] N. Rosenthal,et al. A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair , 2009, Proceedings of the National Academy of Sciences.
[85] R. Holmdahl,et al. Macrophages suppress T cell responses and arthritis development in mice by producing reactive oxygen species. , 2007, The Journal of clinical investigation.
[86] G. Schmid-Schönbein,et al. Chronic venous disease. , 2006, Minerva cardioangiologica.
[87] C. McCollum,et al. Expression of nitric oxide synthase isoforms and arginase in normal human skin and chronic venous leg ulcers , 2000, The Journal of pathology.
[88] J. M. Cousin,et al. Glucocorticoids promote nonphlogistic phagocytosis of apoptotic leukocytes. , 1999, Journal of immunology.
[89] N. Van Rooijen,et al. Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis , 2007, The Journal of experimental medicine.
[90] J. Simon,et al. Expression of the adhesion molecules ICAM-1, VCAM-1, and E-selectin and their ligands VLA-4 and LFA-1 in chronic venous leg ulcers. , 1996, Journal of the American Academy of Dermatology.
[91] E. Zandi,et al. Signaling role of intracellular iron in NF-kappaB activation. , 2003, The Journal of biological chemistry.
[92] S. Gordon,et al. Monocyte and macrophage heterogeneity , 2005, Nature Reviews Immunology.
[93] R. Tarnuzzer,et al. Biochemical analysis of acute and chronic wound environments , 1996, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.