Macrophage plasticity and polarization in tissue repair and remodelling
By A. Mantovani, Subhra K. Biswas, M. Galdiero, A. Sica, M. Locati. Journal of Pathology, 2013
2,334 citations recorded by the source corpus.
Subfields: Immunology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/22bce014b084dd3e67efc3598a7989b72a4cfaa7
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In Immunology
- A. Mantovani
- P. Allavena
- P. Italiani
- D. Boraschi
- L. Cañedo-Dorantes
- Mara Cañedo-Ayala
- Daniel J. Kelly
- A. Cameron
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Biomaterial based modulation of macrophage polarization: A review and suggested design principles (2015, background): “Physical properties such as substrate stiffness, topography, pore size and size of wear debris; chemical properties such as surface chemistry, ligand presentation and release of growth factors; and temporal properties, such as degradation rates, all influence the behavior of cells [8,9].”
- Novel Markers to Delineate Murine M1 and M2 Macrophages (2015, background): “Indeed, M1 macrophages have been implicated in the pathogenesis of several inflammatory conditions including atherosclerosis, diabetes and glomerulonephritis [4,14].”
- Macrophage phenotypes during tissue repair (2013, background): “The concepts of Mp heterogeneity and plasticity have now become widely acknowledged [9, 28, 29], and an appealing model of in vivo Mp activation classifies these cells based on function rather than expression of phenotypic “markers” [9].”
- The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “It is conceivable that chemotherapeutic agents elicit a misdirected macrophage-orchestrated tissue repair response by causing tissue damage in the tumor (Mantovani et al., 2013), which may and chemokine repertoire (e.”
- The Metabolic Signature of Macrophage Responses (2019, background): “They express high levels of mannose receptor (CD206), the decoy receptor IL-1R as well as the IL-1R antagonist, and produce pro-fibrotic factors such as the transforming growth factor beta (TGF-β) and insulin-like growth factor 1 (IGF-1), thus actively suppressing inflammation and promoting repair (”
- From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “Healing MΦb All tissues Branched morphology, angiogenesis (142) Cancer, fibrosis, epithelial hyperplasia (91)”
- Neuroinflammation and M2 microglia: the good, the bad, and the inflamed (2014, background): “One additional type of M2 activated cell, the so-called tumor-associated macrophage, has recently been recognized [52].”
- Mesenchymal stromal cells: sensors and switchers of inflammation. (2013, positive): “…proinflammatory cytokines, M2 macrophages secrete a combination of cytokines (including high levels of IL-10 and TGF-b1 and low levels of IL-1, IL-6, TNF-a, and IFN-g) that together exert an anti-inflammatory effect and allow tissue regeneration following inflammation (Mantovani et al., 2013).”
- Macrophage plasticity, polarization, and function in health and disease (2018, background): “During resolution, M2 macrophages are a major source of lipid mediators and produce anti-inflammatory cytokines, IL-10 and TGF-β involved in tissue resolution (Das et al., 2015; Ginhoux & Jung, 2014; Hinz et al., 2012; Mantovani et al., 2013).”
- The Pathogenesis of Cardiac Fibrosis (2013, neutral): “Macrophages are known to exhibit considerable functional plasticity and to respond to changes in their microenvironment by modulating their cytokine and growth factor expression profile [64].”
- Macrophage Polarization in Physiological and Pathological Pregnancy (2019, background): “Macrophages contribute to the process of infection prevention, tissue repairing, angiogenesis and immunomodulation (5, 20).”
- Titanium Surface Characteristics, Including Topography and Wettability, Alter Macrophage Activation (2015, background): “The M1 activation is a pro-inflammatory response responsible for rapid immune activation in the presence of microbiological or other acute threats [13], characterized by high levels of interleukin IL-1β, IL-6, and TNFα [9, 10, 13].”