An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice.

By A. Sindrilaru, T. Peters, S. Wieschalka, C. Baican, A. Baican, H. Peter, A. Hainzl, S. Schatz, Yu Qi, A. Schlecht and 4 more. Journal of Clinical Investigation, 2011

983 citations recorded by the source corpus.

Subfields: Epidemiology, Rehabilitation

View Paper: https://www.semanticscholar.org/paper/0818ad3d9db724311ad2b07c462ef036e3452904

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. A. Sica
2. Ava J Boutilier
3. A. Mantovani
4. Sherine F. Elsawa
5. M. Perretti
6. Luke A. O'Neill

In Rehabilitation

1. Paul Martin
2. S. Eming
3. M. Tomic‐Canic

Citations in the corpus

• Sequential delivery of immunomodulatory cytokines to facilitate the M1-to-M2 transition of macrophages and enhance vascularization of bone scaffolds (2014, positive): “Macrophages also control healing by influencing the behavior of other cell types, includingfibroblasts in cutaneouswoundhealing [34,35], neurons in spinal cord repair [36,37] osteoblasts in bone defects [38,39], and myogenic cells in skeletal muscle injury [19].”
• Transition from inflammation to proliferation: a critical step during wound healing (2016, background): “For example, iron overload drives macrophages into an unrestrained pro-inflammatory M1activation state, and iron-overloaded macrophages have been detected in human chronic venous ulcers [63, 64].”
• Metabolic Reprograming in Macrophage Polarization (2014, background): “For instance, patients presenting with chronic venous ulcers suffer from chronic inflammation as a result of failing to switch from M1 macrophages to M2 (36).”
• Resolution of inflammation: an integrated view (2013, positive): “Recent work points towards a critical role of alternatively activated macrophages (Lucas et al, 2010; Saclier et al, 2013; Sindrilaru et al, 2011), which secrete anti-inflammatory and reparative mediators including IL1 receptor antagonist, IL10, TGF-b and VEGF.”
• The Role of Macrophages in Acute and Chronic Wound Healing and Interventions to Promote Pro-wound Healing Phenotypes (2018, background): “…it is possible that some wound macrophages have some shared characteristics, especially in regards to Mhem, as hemoglobin-haptoglobin receptor (CD163) expression and cellular regulation of iron are associated with wound healing (Cairo et al., 2011; Sindrilaru et al., 2011; Evans et al., 2013).”
• Wound repair and regeneration: Mechanisms, signaling, and translation (2014, positive): “It has been shown that increased proinflammatory cellular infiltrates composed largely of neutrophils and macrophages contribute to delayed healing in chronic ulcers (27, 28).”
• Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “In contrast, wounds that do not heal within 3 months are considered chronic (Werdin et al., 2009) and persistent macrophage activation is a hallmark of this chronic condition (Sindrilaru et al., 2011).”
• TNF and increased intracellular iron alter macrophage polarization to a detrimental M1 phenotype in the injured spinal cord. (2014, positive): “A similar population of iron-containing macrophages with mixed M1/M2 proinflammatory phenotype was also found in chronic skin ulcers, in which they cause tissue damage (Sindrilaru et al., 2011).”
• Diabetic Wound-Healing Science (2021, background): “…are characterized by the non-resolving inflammation phase, where a large number of neutrophils and macrophages are found in the wound bed [85,88,89], as well as the chronic release of proinflammatory cytokines including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)- α, and plasma C…”
• Macrophages in Tumor Microenvironments and the Progression of Tumors (2012, background): “, TNF-α, IL-1, IL-6, IL-12, and IL-23) and increase their concentrations of superoxide anions, oxygen radicals, and nitrogen radicals [8, 9].”