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Macrophage phenotypes during tissue repair
Open accessAbstract
Review on tissue repair and M1-like to M2a-like macrophages, exhibiting important differences from in vitro phenotypes. Mp are crucial for tissue repair and regeneration but can also contribute to tissue damage and fibrosis. Mp can adopt a variety of functional phenotypes in response to different stimuli; two of the best-characterized in vitro phenotypes are a proinflammatory “M1” phenotype, produced by exposure to IFN-γ and TNF-α, and an anti-inflammatory “M2a” phenotype, produced by IL-4 or IL-13. M2a Mp are frequently termed “wound healing” Mp, as they express factors that are important for tissue repair. This review will summarize current knowledge of Mp phenotypes during tissue repair and will argue that these in vivo Mp populations are heterogeneous and temporally regulated and do not conform to existing, in vitro-defined M1 or M2 phenotypes. Mp during the early stages of tissue repair exhibit a more proinflammatory phenotype than their later counterparts, which in turn may exhibit some M2a-associated characteristics. However, phenotypic markers that appear to be coregulated in cultured Mp can be expressed independently of each other in vivo. Additionally, M1- and M2-associated markers may be expressed simultaneously by actual tissue-repair Mp. Improved understanding of Mp phenotypes and their regulation may assist in generation of novel therapies based on manipulating Mp function to improve healing.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that macrophages present during in vivo tissue repair are heterogeneous and temporally regulated and do not conform to the in vitro-defined M1 or M2a phenotypes. Early-repair macrophages are more proinflammatory than later ones, but neither population matches a discrete cultured phenotype.
Key findings
- M2a macrophages are widely termed "wound-healing" macrophages because IL-4/IL-13 treatment up-regulates TGF-β, arginase, and ECM components, but the review argues this nomination is "an oversimplification at best and likely not warranted."
- In a mouse sponge-implantation wound model, macrophages produced TGF-β despite no detectable IL-4 or IL-13 in wound fluids or cells and no Stat6 phosphorylation, indicating M2a activation is sufficient but not necessary for TGF-β production.
- M2a-associated markers are regulated independently in vivo: in murine subcutaneous wounds, CD206 increased with time, Ym1 was highest at 1 day and then decreased, and dectin-1 remained constant; CD206 expression was similar among TNF-α-high, -low, or -negative macrophages.
- iNOS expression by tissue-repair macrophages is context-dependent: highest at 1 day in mouse kidney ischemia-reperfusion, but only 10–15% of wound macrophages were iNOS-positive at peak in rat excisional skin wounds, and mouse muscle macrophages expressed iNOS after chemical injury but not after laceration.
- Human M2a macrophages or monocytes do not express arginase (unlike rodent), and human iNOS activity is much lower or absent (~20 nmol nitrite/10⁶ cells/24 h in rodent M1 macrophages; often undetectable in human).
Methods
- Narrative review summarizing current knowledge of macrophage phenotypes during tissue repair, drawing on cited in vitro and in vivo studies across skin, skeletal muscle, liver, kidney, and peritoneum.
- Compares in vitro-defined M1/M2a/b/c phenotypes with in vivo tissue-repair macrophage populations, including a summary table (Table 1) of activators, cytokines, iNOS, and markers (CD206, dectin-1, Ym1) across early and late repair.
- Includes some unpublished results from the authors' laboratory (mouse skeletal muscle laceration and chemical injury models).
Limitations
- Stated: many studies reporting M2a markers during repair did not verify that markers were expressed by macrophages rather than other cell types; whole-tissue cytokine content cannot determine macrophage phenotype; direct quantitative comparisons of cytokine production between cultured M1/M2a macrophages and in vivo tissue-repair macrophages are currently unavailable.
- Stated: rodent and human macrophages do not exhibit entirely similar responses to in vitro activation, and whether species-dependent differences exist in in vivo repair is undetermined.
- Evident from the text: several key supporting observations are unpublished results from the authors' own laboratory, and the review notes that the factors regulating in vivo macrophage phenotype "remain to be elucidated."
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Claims the paper makes
36 Own interpretation · 33 Not checked yet · 11 No basis given · 1 Own result
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Mp can adopt a variety of functional phenotypes in response to different stimuli; two of the best-characterized in vitro phenotypes are a proinflammatory”
§ Macrophage phenotypes during tissue repair > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Mp, in particular, are known to be essential to regeneration, repair, and remodeling in numerous tissues [1][2][3][4][5].”
§ Macrophage phenotypes during tissue repair > Introduction
What the sources say
- Not checked yetcites [1][2][3][4][5]
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, chronic inflammation and persistent Mp accumulation are often associated with tissue destruction and fibrosis [6 -8].”
§ Macrophage phenotypes during tissue repair > Introduction
What the sources say
- Not checked yetcites [6] Moreira, 2011, Macrophages in allergic asthma: fine-tuning their pro- and anti-inflammatory actions for disease resolution, J. Interfron Cytokine Res. source
- Not checked yetcites [7] Moyer, 2011, Regeneration versus fibrosis in skeletal muscle, Curr. Opin. Rheumatol. source
- Not checked yetcites [8] Murray, 2011, Protective and pathogenic functions of macrophage subsets, Nat. Rev. Immunol. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The M1-associated cytokines IL-1, TNF-␣, IL-6, and IL-12 are expressed by Mp during the first few hours to days after acute injury in numerous tissues, including skin [33,60,61], liver [62], kidney [63], and skeletal muscle [57,64].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
- Not checked yetcites [60] Mirza, 2011, Dysregulation of monocyte/macrophage phenotype in wounds of diabetic mice, Cytokine source
- Not checked yetcites [61] Sindrilaru, 2011, An unrestrained pro-inflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice, J. Clin. Invest. source
- Not checked yetcites [62] Karlmark, 2010, The fractalkine receptor CX3CR1 protects against liver fibrosis by controlling differentiation and survival of infiltrating hepatic monocytes, Hepatology source
- Not checked yetcites [63] Lee, 2011, Distinct macrophage phenotypes contribute to kidney injury and repair, J. Am. Soc. Nephrol. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, available evidence indicates that M1 and M2a/b/c are not discrete Mp differentiation states but instead represent convenient but limited and arbitrary in vitro-defined reference points on a time-dependent and multidimensional continuum of possible Mp phenotypes and functions [9].”
§ Macrophage phenotypes during tissue repair > EVOLVING Mp ACTIVATION PARADIGMS
What the sources say
- Not checked yetcites [9] Mosser, 2008, Exploring the full spectrum of macrophage activation, Nat. Rev. Immunol. source
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the presence of arginase or even of arginase-expressing Mp does not necessarily imply that IL-4/IL-13-induced M2a Mp are present in a tissue.”
§ Macrophage phenotypes during tissue repair > EVIDENCE FOR M2a Mp AS TISSUE-REPAIR Mp
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Importantly, in contrast to rodent Mp, human M2a Mp or monocytes do not express arginase [36,37].”
§ Macrophage phenotypes during tissue repair > EVIDENCE FOR M2a Mp AS TISSUE-REPAIR Mp
What the sources say
- Not checked yetcites [36] Munder, 2005, Arginase I is constitutively expressed in human granulocytes and participates in fungicidal activity, Blood source
- Not checked yetcites [37] Raes, 2005, Macrophage galactose-type C-type lectins as novel markers for alternatively activated macrophages elicited by parasitic infections and allergic airway inflammation, J. Leukoc. Biol. source
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This review will address recent advances in our understanding of Mp phenotypes during tissue repair and will argue that the Mp populations that participate in tissue repair are not analogous to in vitro M2a Mp.”
§ Macrophage phenotypes during tissue repair > Introduction
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, phenotypic markers that appear to be coregulated in cultured Mp can be expressed independently of each other in vivo.”
§ Macrophage phenotypes during tissue repair > Abstract
hedged- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Mp during the early stages of tissue repair exhibit a more proinflammatory phenotype than their later counterparts, which in turn may exhibit some M2a-associated characteristics.”
§ Macrophage phenotypes during tissue repair > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: The phases of tissue repair (inflammation, proliferation, remodeling) are universal across tissues.
- Probably not a substantial claim. 5
- It may state two separate claims as one. 24
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Similarly, after mouse skeletal muscle laceration, Mp expression of TGF- mRNA and IL-10 mRNA appears to peak early, ϳ3 days postinjury (unpublished results).”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Studies from our own laboratory have produced contradictory data in two different mouse muscle injury models: skeletal muscle Mp express iNOS mRNA at 5 days after chemically induced injury [57] but do not express iNOS at any time-point after laceration injury (unpublished results).”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [57] Cheng, 2008, Endogenous interferon-γ is required for efficient skeletal muscle regeneration, Am. J. Physiol. Cell. Physiol. source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“For instance, in a mouse wound-healing model, Mp expression of the M2a marker CD206 does not require IL-4 or IL-13 and does not correlate, negatively or otherwise, with TNF-␣ production [33].”
§ Macrophage phenotypes during tissue repair > EVIDENCE FOR M2a Mp AS TISSUE-REPAIR Mp
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“two of the best-characterized in vitro phenotypes are a proinflammatory”
§ Macrophage phenotypes during tissue repair > Abstract
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“M2a Mp are frequently termed”
§ Macrophage phenotypes during tissue repair > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The M1 activator IFN-␥ is up-regulated rapidly after injury to skeletal muscle and skin and is required for proper healing of these tissues [55][56][57][58].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [55][56][57][58]
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, whereas it is clear that treatment of cultured Mp with particular cytokines produces characteristic phenotypes, the presence of one or a few phenotypic markers in vivo does not demonstrate that the Mp was activated by the associated cytokine or that other aspects of the phenotype induced by that cytokine will also be present.”
§ Macrophage phenotypes during tissue repair > EVIDENCE FOR M2a Mp AS TISSUE-REPAIR Mp
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Wound healing is thus not a single, well-defined function of Mp but comprises its own spectrum of overlapping functions, including phagocytosis, secretion of cytokines and growth factors, as well as matrix remodeling, all of which may be performed by Mp of different phenotypes.”
§ Macrophage phenotypes during tissue repair > EVOLVING Mp ACTIVATION PARADIGMS
hedgedconditional- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In numerous physiological and pathological states, Mp exhibit extensive heterogeneity and plasticity, and tissue repair is no exception.”
§ Macrophage phenotypes during tissue repair > Introduction
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, existing data on anti-inflammatory cytokine production suggest that Mp may become more M2a-like as repair progresses, although this transition may not happen in all situations.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: The phases of tissue repair (inflammation, proliferation, remodeling) are universal across tissues.
In the paper
“In contrast, in a mouse sponge-implantation model of skin wounding, deletion of IL-4R␣ has no effect on Mp phenotype, and IL-4 and IL-13 are not detected in wound cells or fluids at any time, indicating that despite their predominantly anti-inflammatory cytokine profile, these cells are not bona fide M2a Mp [33].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
hedged- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, during mouse skin wound healing, Mp expression of TGF- mRNA and protein increases over the first 7-10 days postinjury, whereas proinflammatory cytokine production decreases [33,60], consistent with the expression of an M2a-like phenotype during the later stages of repair.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Similarly, after peritoneal incisional wounding, peritoneal exudate cells transiently express elevated Ym1 and FIZZ1 mRNA, although this cell population contains lymphocytes and neutrophils in addition to Mp [70], and each of these cell types could express one or both genes [76,77].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [70] Loke, 2007, Alternative activation is an innate response to injury that requires CD4+ T cells to be sustained during chronic infection, J. Immunol. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Seven days after photochemical injury to the liver, CD206ϩ cells are observed near the border of the injured site [68], although these cells were not verified specifically as Mp, and no other time-points were examined.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [68] Kawao, 2011, Urokinase-type plasminogen activator contributes to heterogeneity of macrophages at the border of damaged site during liver repair in mice, Thromb. Haemost. source
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Collectively, data from these studies indicate that the M2a markers CD206, Ym1, and dectin-1 can be regulated independently of each other in skin-wound Mp and can be coexpressed with M1-associated or proinflammatory genes and proteins.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In murine skeletal muscle, however, Mp expression of TGF- and IL-10 mRNA increases over the first few days after toxin-induced injury, peaks during the intermediate stages of healing, and then declines sharply, despite continued presence of Mp within the healing muscle [65].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [65] Perdiguero, 2011, p38/MKP-1-regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair, J. Cell Biol. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, Mp during skin wound healing exhibit a heterogeneous and temporally regulated phenotype that does not conform strictly to M1/M2 categorization [33].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
plain- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Tissue repair in mice is representative of tissue repair in humans.
- Rests on an assumption: The phases of tissue repair (inflammation, proliferation, remodeling) are universal across tissues.
In the paper
“However, although CD206, Ym1, and dectin-1 are expressed by murine subcutaneous wound Mp at 1, 3, and 7 days postinjury [33], these three M2a-associated proteins exhibit entirely different temporal patterns: CD206 increases somewhat with time, whereas Ym1 is expressed most highly at 1-day postinjury and then decreases, and dectin-1 expression remains constant [33].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Numerous studies in other tissues have reported that M2a markers are present during tissue repair, but many of these studies have not determined whether these markers are expressed by Mp or by other cell types, and any conclusions drawn regarding Mp phenotype are therefore dubious.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition to proinflammatory cytokine production, robust expression of iNOS is a hallmark of M1 activation in rodent Mp [14], although iNOS activity in human Mp appears to be much lower or absent entirely (ϳ20 nmol nitrite/10 6 cells/24 h in rodent M1 Mp; often undetectable in human Mp) [66].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, as IL-4/-13 activation is not always required for up-regulation of IL-10 and TGF- [33], the presence of other aspects of the M2a phenotype should not be inferred from cytokine expression alone.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [33] Daley, 2010, The phenotype of murine wound macrophages, J. Leukoc. Biol. source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“However, IL-4 gene expression is elevated from 1 to 7 days in rat skin wounds [56], and protein expression is elevated between 12 h and 10 days in human skin wounds (peak ϳ12 pg/mg protein in injured skin vs. nearly undetectable in uninjured) [58]; IL-4 protein is present at similar levels in infarcted rat myocardium [72].”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
What the sources say
- Not checked yetcites [56] Miao, 2012, Diabetes-impaired wound healing and altered macrophage activation: a possible pathophysiologic correlation, Wound Repair Regen. source
- Not checked yetcites [58] Takamiya, 2008, Simultaneous detection of eight cytokines in human dermal wounds with a multiplex bead-based immunoassay for wound age estimation, Int. J. Legal Med. source
- Not checked yetcites [72] Fraccarollo, 2008, Immediate mineralocorticoid receptor blockade improves myocardial infarct healing by modulation of the inflammatory response, Hypertension source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In short, tissuerepair Mp exhibit complex and heterogeneous phenotypes that change throughout the repair process and do not correspond to existing, in vitro -defined categories.”
§ Macrophage phenotypes during tissue repair > CONCLUDING REMARKS
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Whereas Mp are known to promote tissue-repair functions such as wound debridement, cell proliferation, angiogenesis, and matrix remodeling, much remains to be learned about the mechanisms by which Mp accomplish these functions.”
§ Macrophage phenotypes during tissue repair > CONCLUDING REMARKS
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A proinflammatory-to-anti-inflammatory transition may indeed occur in many situations, although this appears to be context-dependent”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whereas Mp during the early stages of tissue repair seem to present a more generally proinflammatory profile than their later counterparts, early Mp may lack iNOS expression or may express CD206, Ym1, and IL-10 in addition to proinflammatory cytokines, indicating that these early-repair Mp do not exhibit an entirely M1 phenotype.”
§ Macrophage phenotypes during tissue repair > CONCLUDING REMARKS
hedged- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Given the growing belief that M2a Mp participate in tissue repair, surprisingly few studies have actually examined Mp-specific expression of M2a-associated genes or proteins in vivo or performed quantitative comparisons of cytokine production by cultured M1/M2a Mp versus in vivo tissuerepair Mp.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Similarly, whereas many potential modulators of Mp activation have been identified in vitro, the actual factors that regulate Mp phenotype during tissue repair remain to be elucidated.”
§ Macrophage phenotypes during tissue repair > CONCLUDING REMARKS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Tissue repair in mice is representative of tissue repair in humans.
“In mouse and human skin wounds and in injured mouse kidney, Mp expression of CD206 increases during the later stages of repair [33,60,61,63].”
The paper relies on this without support.
The phases of tissue repair (inflammation, proliferation, remodeling) are universal across tissues.
“Across diverse tissues, repair after injury occurs in overlapping phases of inflammation, proliferation, and remodeling.”
Claims other papers make about this one
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In the citing paper
“The classical model distinguishes two major polarization phenotypes, which represent a continuum, providing a balance between the pro‐ and anti‐inflammatory responses by alternating between classically (M1) or alternatively (M2) activated macrophages.[ 37 , 38 ]”
From Unraveling and Harnessing the Immune Response at the Cell–Biomaterial Interface for Tissue Engineering Purposes (2024) · cites this paper as [37]
Experimental — accuracy not yet measuredIn the citing paper
“Recent studies have shown that Mp phenotypes change over the different phases of tissue repair and that the sequential appearance of these phenotypes may be required for efficient repair (11,14,29,49,50).”
From Sustained Inflammasome Activity in Macrophages Impairs Wound Healing in Type 2 Diabetic Humans and Mice (2014) · cites this paper as [50]
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In the paper
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
“TGF- increases with time (skin); IL-10 time course not known.”
§ Macrophage phenotypes during tissue repair > Mp PHENOTYPES DURING TISSUE REPAIR AND FIBROSIS
“In murine skeletal muscle, however, Mp expression of TGF- and IL-10 mRNA increases over the first few days after toxin-induced injury, peaks during the intermediate stages of healing, and then declines sharply, despite continued presence of Mp within the healing muscle [65].”
Citations
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Cited by
Sorted by citations
Items 501–600 of 654
He, Y., Hu, J., Ma, A., Du, P., Yang, M., Xiong, X., & Deng, Y. (2026) · Journal of Inflammation Research · doi:10.2147/jir.s566523 · Cited by 5
“84 Macrophages are key cells in regulating skin wound healing, and the specific removal of macrophages severely impairs the healing process.”
Caloric restriction protects from acute and chronic kidney injury by inhibiting monocyte recruitment
Molinari, P., Verlato, A., Noble, J., Alibrandi, S., Bin, S., Ferrari, K. L., Malvezzi, P., Alfieri, C., Castellano, G., Perin, L., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113094 · Cited by 5
“4,8,9 During the initial phases, activated macrophages exhibit robust phagocytic activity, allowing for the clearance of apoptotic bodies and necrotic cellular debris.”
Walsh, C. M., Colbert, R., Reynolds, J. R., Dunne, E., Aiyegbusi, E. D., O'Carroll, R., Wychowaniec, J. K., Masuda, T., Knobeloch, K., Prinz, M., et al. (2025) · Bioactive Materials · doi:10.1016/j.bioactmat.2025.07.018 · Cited by 6
“IL-10 stimulates M2c polarisation which is defined by increased transforming growth factor beta (TGF-β ) secretion to promote angiogenesis and tissue remodelling [18,19].”
Passariello, R., Imparato, G., Casale, C., Urciuolo, F., & Netti, P. A. (2025) · Acta Biomaterialia · doi:10.1016/j.actbio.2025.08.027 · Cited by 6
The osteoimmunomodulatory effect of nanostructured TiF x /TiO x coating on osteogenesis induction
Chen, M., Hu, J., Zhang, E., Hu, J., Wang, X., & Qin, G. W. (2021) · Biomedical Materials · doi:10.1088/1748-605x/ac0863 · Cited by 4
“Appropriate macrophage activation is beneficial for bone healing [21, 22], while an improper reaction can exacerbate inflammation and disrupt healthy tissue-implant integration [23].”
Cao, X., Lu, R., Wang, X., Wang, C., Zhao, Y., Sun, Y., & Chen, S. (2022) · Journal of Nanomaterials · doi:10.1155/2022/2650421 · Cited by 4
Yoon, C., Kim, H. K., Ham, Y. S., Gil, W. J., Mun, S., Cho, E., Yuk, J., & Yang, C. (2024) · Science Advances · doi:10.1126/sciadv.adq0101 · Cited by 4
“…we observed a dose-dependent increase in cd80 , cd86 , and iNOS expression following treatment with TgMIF WT compared to TgMIF K76D. cd206 is commonly expressed on tissue-resident macrophages that exhibit an M2-polarized phenotype, often associated with a reparative function ( 44 , 45 ).”
The VASP Road to NAFLD: A Macrophage Detour
Lastra, G., Manrique, C. M., Jia, G., & Sowers, J. R. (2015) · Diabetes · doi:10.2337/db15-0551 · Cited by 4
“Conversely, the antiinflammatory M2 phenotype secretes preferentially CD206, arginase1, and IL-10 (8).”
BackgroundHost Defense Antibacterial Effector Cells Influenced by Massive Burns
Kobayashi, M., Toliver-Kinsky, T. E., & Suzuki, F. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-47661-4.00020-4 · Cited by 4
Toyama, N., Tsuchiya, S., Kamio, H., Okabe, K., Kuroda, K., Okido, M., & Hibi, H. (2020) · Journal of Materials Science Materials in Medicine · doi:10.1007/s10856-020-06412-7 · Cited by 4
Krupek, T., da Silva, M. A. R. C. P., ́Ana, D. D. M. G. S., et al. (2016) · Brazilian Journal of Pharmaceutical Sciences · doi:10.1590/s1984-82502016000300021 · Cited by 4
Zemans, R. L., & Downey, G. P. (2015) · Elsevier eBooks · doi:10.1016/b978-1-4557-3383-5.00015-4 · Cited by 4
Anders, C. B., Lawton, T., Smith, H. L., Garret, J., Doucette, M. M., & Ammons, M. C. B. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.03.10.985788 · Cited by 4
“Observed to be ineffective at bacterial clearance [21], M2b MΦs display characteristics indicative of a tissue remodeling functional phenotype which include ECM synthesis and angiogenic potential [22].”
BackgroundNg, K. L. B., Lin, Y.-N., Chen, W.-Y., Wu, Y., Huang, S., Lee, S., Chen, R., & Kuo, Y. (2025) · Journal of Wound Care · doi:10.12968/jowc.2023.0318 · Cited by 4
Effect of rhGM-CSF in Promoting Wound Healing via Macrophage Immunomodulation
Zhang, X., Zhao, Z., Gong, S., Yi, C., Xu, A., Tao, J., Yu, X., & Shao, S. (2025) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaf480 · Cited by 3
Dynamic Interplay Between Smooth Muscle Cells and Macrophages in Vascular Disease
Iwata, H., & Aikawa, M. (2015) · InTech eBooks · doi:10.5772/61089 · Cited by 4
“During the repair process after tissue injury, M2 cell may promote fibrosis [102], [103].”
BackgroundControlled release of pioglitazone from biodegradable hydrogels to modify macrophages phenotype
Sato, K., Sakai, S., Kishi, K., & Tabata, Y. (2015) · Inflammation and Regeneration · doi:10.2492/inflammregen.35.086 · Cited by 3
The Role of Instrumentation in the Healing Process of Spinal Tuberculosis: An Experimental Study
Risantoso, T., Hidayat, M., Suyuti, H., et al. (2021) · Open Access Macedonian Journal of Medical Sciences · doi:10.3889/oamjms.2021.6065 · Cited by 3
“M2 anti-inflammatory response is shown by high level of interleukin (IL)-4, IL-10, and Transforming growth factor beta 1 (TGF-βl) [12], [13], [14].”
BackgroundSuzuki, C., Komiya, T., Inoue, H., Yoshimoto, T., & Matsumura, H. (2021) · International Wound Journal · doi:10.1111/iwj.13706 · Cited by 2
“M1 macrophages induce the inflammatory reaction required for tissue engraftment, and they are involved in the scavenging of necrotic adipose tissue, whereas M2 macrophages are involved in tissue repair, and both M1 and M2 macrophages carry out an important role in the process of adipose tissue remodelling and engraftm…”
BackgroundBiomaterials modulate macrophage polarization and inflammatory responses
Zheng, W., Huang, H., Guo, F., Yuan, C., & Zhou, Q. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-822368-0.00006-2 · Cited by 4
Kanwar, M., Dey, R., Maiti, S., Banerjee, A., & Bishayi, B. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2022.109654 · Cited by 3
Malaviya, R., Meshanni, J. A., Sunil, V. R., et al. (2024) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2024.116908 · Cited by 3
“TGF-β 1 plays a role in tissue remodeling and wound healing, as well as in fibrogenesis (Novak and Koh, 2013; Ramirez et al., 2014).”
Lu, H., Chen, T., Zhang, X., et al. (2015) · Journal of Craniofacial Surgery · doi:10.1097/scs.0000000000002122 · Cited by 3
“conducive to remove of debris to initiate tissue repair.(8) Therefore, the white blood cells in PRP displayed a key role in wound healing through immune-modulating effects.”
BackgroundLiu, Y., Zhang, W.-S., Tang, Z.-H., Ye, D.-D., Su, S., Zhang, S.-M., & Qiu, J. (2021) · Biomedical Materials · doi:10.1088/1748-605x/ac3620 · Cited by 4
Almahrog, A. J., Radwan, L. R. S., El-Zehery, R. R., et al. (2016) · Journal of Oral Biology and Craniofacial Research · doi:10.1016/j.jobcr.2015.12.009 · Cited by 3
“mental cues by adopting either ‘‘classically’’ activated (M1) proinflammatory or ‘‘alternatively’’ activated (M2a, M2b, M2c, and M2d) wound healing phenotypes.(8,9) M2a macrophages secrete the highest levels of PDGF-B, a chemoattractant stabilizing pericytes, and also promote anastomosis of sprouting endothelial cells…”
BackgroundFujihara, Y., Yamanegi, K., Nagasawa, Y., Yoshida, A., Goto, Y., Kumanishi, S., Futani, H., Fukunishi, S., Yoshiya, S., & Nishiura, H. (2021) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2020.100898 · Cited by 3
“Circulating lymphocytes are believed to infiltrate into local foci at the inflammation phase of acute wound healing for identifying foreign antigens on M1 macrophages activated by type II interferon (IFN gamma) in the mature immune system [4].”
BackgroundMohtadi, M. E. (2019) · e-space (Manchester Metropolitan University) · Cited by 3
Cockrell, C., Yoram Vodovotz, B., Zamora, R., & An, G. C. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.04.595972 · Cited by 3
Sapudom, J., Tipay, P. S., & Teo, J. C. M. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.29.605566 · Cited by 3
Palmieri, A., Pellati, A., Lauritano, D., Lucchese, A., Carinci, F., Scapoli, L., & Martinelli, M. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111441 · Cited by 2
“…researchers have hypothesized that the persistence of pro-inflammatory M1 macrophages and their reactive products may cause tissue damage that is compensated for through M2 polarization aimed at restoring the pre-inflammatory state and tissue healing, possibly with fibrosis formation [18,19].”
BackgroundEremichev, R. Y., & Макаревич, П. И. (2024) · Tsitologiya · doi:10.31857/s0041377124030011 · Cited by 2
Obara, K., Baba, K., Shirai, K., Hamada, Y., Arakawa, N., Hasegawa, A., Takaoka, N., Aki, R., & Hoffman, R. M. (2025) · Cell Cycle · doi:10.1080/15384101.2025.2508112 · Cited by 2
“Increasing evidence suggests that M1 (CD86+, CD80+) is the predominant macrophage population in the early stage of scar formation (inflammatory and early proliferative stage), whereas M2 (CD206+, CD163+) is the main population in the late stage (late proliferative and remodeling stage) [56,57].”
Immunomodulation and iron dysregulation: exploring their roles in the pathogenesis of osteoarthritis
Yang, D., Ruan, Y., Zheng, S., Xu, W., & Hao, J. (2025) · BMC Medical Genomics · doi:10.1186/s12920-025-02206-4 · Cited by 3
“In contrast, M2 macrophages are considered anti-inflammatory and play a role in tissue repair and resolution of inflammation by secreting cytokines like IL-10 and TGF-β [22, 23].”
Du, J., Huang, S., Di, A., Wei, N., Cui, Y., & Zhang, Y. (2026) · Discover Oncology · doi:10.1007/s12672-026-04730-w · Cited by 2
Role of Hepatic Macrophages in Acute and Chronic Injury and Repair
Bin-Kamran, A., Mishra, A. K., Reddy, S., Reddy, N., Khan, R., & Kruger, A. K. (2022) · Georgetown Medical Review · doi:10.52504/001c.34718 · Cited by 2
Chen, S., Wang, Y., Liu, Y., Bai, L., Li, F., Wu, Y., Xie, X., Zhang, N., Zeng, C., Zhang, L., et al. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1145675 · Cited by 2
“These data suggest that CLP surgery induced the IL-6, IL-1β, TNF-α, and MCP-1 mRNA levels in the mice kidneys, while DHT pretreatment reversed these changes (Figures 5E–”
BackgroundInfluentialSerack, F. E., Fennell, K. A., Iliopoulos, C., Walker, J. T., Ronald, J. A., Amsden, B. G., Hess, D. A., & Flynn, L. E. (2024) · Journal of Biomedical Materials Research Part A · doi:10.1002/jbm.a.37800 · Cited by 2
Wang, X., Wang, T., Zhu, D., Wang, J., & Han, W. (2024) · Clinical & Experimental Immunology · doi:10.1093/cei/uxae105 · Cited by 2
Nash, V. A., Cortés-Troncoso, J., Chua, P. E., & Spiller, K. L. (2025) · Journal of Controlled Release · doi:10.1016/j.jconrel.2025.113943 · Cited by 3
“Macrophages are critical regulators of all other cells throughout every stage of the healing process, including the response to implanted biomaterials (reviewed in [1,2]).”
Insights From Amniotic and Umbilical Cord Mesenchymal Stem Cells in Wound Healing
Shen, N., Wu, Y., Yang, K., Xv, X., Lü, G., Pan, R., & Yang, J. (2025) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.70679 · Cited by 2
The importance of targeting inflammation in skin regeneration
Schrementi, M. E., Chen, L., & DiPietro, L. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-810545-0.00011-5 · Cited by 3
Modulation of Inflammatory Dynamics by Insulin to Promote Wound Recovery of Diabetic Ulcers
Kaur, P., & Choudhury, D. (2020) · IntechOpen eBooks · doi:10.5772/intechopen.92096 · Cited by 3
Cutting-edge therapies in the treatment of surgical wounds
Zepeda, J. M., Contreras-Cárdenas, J., Gutiérrez, F. O., Jimenez, M., & Murrieta, A. (2021) · International Surgery Journal · doi:10.18203/2349-2902.isj20214821 · Cited by 2
“The epidermis regains its usual thickness as superficial cell differentiation gives way to a mature epidermal architecture with superficial keratinization.(6,8) In the second week, there is a constant accumulation of collagen and fibroblastic proliferation, as well as a decrease in leukocyte infiltrate, edema and vasc…”
BackgroundZdziennicka, J., Wessely-Szponder, J., Starobrat, G., & Junkuszew, A. (2021) · Animals · doi:10.3390/ani11123569 · Cited by 2
Immune Functions of the M2 Macrophages: Host Defense, Self-tolerance, and Autoimmunity
Rőszer, T. (2020) · Progress in inflammation research · doi:10.1007/978-3-030-50480-9_6 · Cited by 2
Human cell therapy for venous leg ulcers
Slade, H. B., Jacobson, N., & Lu, Y. (2015) · Phlebological Review · doi:10.5114/pr.2015.54032 · Cited by 1
“While colonization of the exposed tissue by bacteria further stimulates the influx of PMN and M1 macrophages [18], thus adding to the inflammatory state, VLU are not acute wounds that become chronic by virtue of becoming “stuck in the inflammatory phase” of normal wound repair [19].”
BackgroundLiu, Y., Liu, P., Zhang, C., et al. (2023) · Medicine · doi:10.1097/md.0000000000034642 · Cited by 1
“[16] M2b macrophages can be induced by the combination of the IgG immune complex and lipopolysaccharide, with high IL-10 and low IL-12 expression, which gives them effective anti-inflammatory properties.[17] M2c macrophages can be induced by IL-10 and TGF-β, regulate anti-inflammatory functions and promote fibrosis.”
BackgroundZhao, J., Zong, Y., Wu, T., Yang, Y., Li, L., Tang, W., Zhao, X., Xie, X., Gao, Y., Zhou, C. H., et al. (2025) · Chemical Engineering Journal · doi:10.1016/j.cej.2025.170005 · Cited by 1
Viana, I. S., Filippo, P. A. D., Carra, G. J. U., Gobbi, F. P., Ribeiro, L. S., Ribeiro, R. B., Petri, F. A. M., Favero, M. L., Ribeiro, L. M. F., de Carvalho, E. C. Q., et al. (2025) · Bioengineering · doi:10.3390/bioengineering12111147 · Cited by 2
“Elevated macrophage recruitment and ongoing inflammation maintained the presence of M1 macrophages (with pro-inflammatory gene expression), leading to sustained TNF-α levels [27], as depicted in Figure 2A,B.”
Sun, C., Zhang, Y., Liu, J., Wei, N., Li, F., Fang, Y., Li, Y., Li, S., Ma, X., Wang, Z., et al. (2025) · Molecular Immunology · doi:10.1016/j.molimm.2025.10.015 · Cited by 1
Bhat, P., Satapathy, A., Yadav, N., Satapathy, A., Chandrakar, K., Satapathy, A., Bhardwaj, S. K., & Patel, N. (2026) · Journal of Drug Delivery and Therapeutics · doi:10.22270/jddt.v16i3.7630 · Cited by 1
Ali, R. H., Faisal, T., Kulkarni, K., Patel, S. N., & Hussain, T. (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1796687 · Cited by 1
“Macrophages, which are a part of the innate response, present a complex inflammatory and anti-inflammatory phenotype (Novak and Koh, 2013).”
Plasmonic fluorescent Ag/C-based nanohybrids for treatment of chemically-induced cutaneous burns
Kuznietsova, H. M., Byelinska, I., Ishchuk, A., et al. (2026) · Biomaterials Science · doi:10.1039/d5bm01540e · Cited by 1
Chen, G., Yin, B., Khan, M. B., Yang, Y., Sun, Q., Zhang, T., Hu, H., & Lin, J. (2026) · Breast Cancer Targets and Therapy · doi:10.2147/bctt.s578930 · Cited by 1
“74,75 M2 polarization can be initiated after an initial inflammatory phase, accompanied by the subsequent emergence of oxidative stress, aiming to mitigate inflammation and facilitate tissue healing and fibrosis.”
Immune dysregulation in chronic diabetic wounds: therapeutic opportunities for healing reprogramming
Yu, W., Li, Q., Wang, J., Fu, J., Hao, Y., Wang, Z., Xu, H., Zhang, M., Zhao, G., & Ma, Y. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1889465 · Cited by 2
“The transition from M1 to M2 macrophage predominance is critical for the progression from the in fl ammatory to the proliferative phase of wound healing (43) (Figure 2).”
Son, K., Kim, S. A., Kang, M., Jo, Y., Kim, C., Park, K., Jung, Y., Kim, T. Y., & Seo, J. (2026) · Burns & Trauma · doi:10.1093/burnst/tkag055 · Cited by 1
Role of macrophages in systemic inflammation: wound healing
Ahmed, M. S., Rahman, M., Matin, M. A., Hossen, M. J., & Sikder, M. H. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-822368-0.00015-3 · Cited by 1
Molecular and Cellular Mechanisms of Water-Filtered IR
Hamblin, M. R. (2022) · Springer eBooks · doi:10.1007/978-3-030-92880-3_23 · Cited by 1
王, 含. (2023) · Advances in Clinical Medicine · doi:10.12677/acm.2023.1381733 · Cited by 1
In silico assessment of CAR macrophages activity against SARS-CoV-2 infection
Amoddeo, A. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e39689 · Cited by 2
“…IL-6 [13] according to ϕ 73 , while the extra contribution from CAR-Ms is accounted for by a L : The last model equation concerns the evolution of IFN-γ , contribution to which includes diffusion according to D IG , production/ activation by CD4 + T-cells [49,50,55] and M1 macrophages [1,4] (10)”
BackgroundAparna, N. S., Sreedevi, A. S., Mohan, M. S., Boban, P. T., & Saja, K. (2024) · Physiology International · doi:10.1556/2060.2024.00432 · Cited by 1
Topical Anti-inflammatory Agents in Wound Care
Chiricozzi, A., & Romanelli, M. (2020) · Updates in clinical dermatology · doi:10.1007/978-3-030-28872-3_6 · Cited by 1
Szabó, G., Saha, B., & Ambade, A. (2018) · Elsevier eBooks · doi:10.1016/b978-0-323-37591-7.00004-5 · Cited by 1
Fungal Recognition and Host Defense Mechanisms
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Review of Ortho-Biologics in Rotator Cuff Repair
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Clinical Features of Pregnant Women and Neonates with COVID-19 in Wuhan: a paired comparison studyPreprint
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BackgroundMacrophage polarity and wound age determinationPreprint
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Mechanisms of Biomaterial-Mediated Cardiac and Esophageal Repair
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Alternatively activated macrophages protect mice during induced intestinal inflammation
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Modulation of Innate Immune Response for Tissue Engineering
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“Of these, M2a macrophages induced by IL-4 and IL-13 are capable of producing TGF-β and arginase, as well as their ability to produce certain ECM components that play a role in tissue-repair; M2b macrophages, which are induced by TLR ligation or immune complexes, promote the production of IL-10 and decreases production…”
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Metadata
- Authors
- Novak, M. L., & Koh, T. J.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Koh, Timothy J
- ORCID
- Koh, Timothy J
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-03-15
- Volume
- 93
- Issue
- 6
- Pages
- 875-881
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- PMC
- PMC3656331
- OpenAlex
- W2159442019
- Semantic Scholar
- 32d24c1f92ce6e25fe1a62057f0c92ea3227742b
- Cited by
- 658
- References
- 85
- Citations by year
- 2026: 29 · 2025: 52 · 2024: 61 · 2023: 47 · 2022: 59 · 2021: 75 · 2020: 50 · 2019: 46 · 2018: 45 · 2017: 47 · 2016: 54 · 2015: 52 · 2014: 29 · 2013: 10
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Department of Defense (#W81XWH-05-1-0159)
- U.S. National Institutes of Health (#R01GM092850)
- American College of Sports Medicine Doctoral Student Research (#2011-03604-00-00)
- University of Illinois at Chicago Graduate College Dean’s Scholar Award
- Topics
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- macrophage phenotype, tissue repair, M1 macrophages, M2 macrophages, wound healing, macrophage heterogeneity, macrophage polarization, inflammatory macrophages, anti-inflammatory macrophages, fibrosis, macrophage markers
- MeSH terms
- Animals, Humans, Macrophages, Phenotype, Regeneration, Wound Healing
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