The DOI matches its Crossref record; 103 of the 105 references it cites were found in a registry or an index; 1 of the 81 sources its claims cite were checked for support.
Immunology of Wound Healing
Open accessAbstract
PURPOSE OF REVIEW: Chronic wounds are a tremendous burden on the healthcare system and lead to significant patient morbidity and mortality. Normal cutaneous wound healing occurs through an intricate and delicate interplay between the immune system, keratinocytes, and dermal cells. Each cell type contributes signals that drive the normal phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This paper reviews how various immunological cell types and signaling molecules influence the way wounds develop, persist, and heal. RECENT FINDINGS: Concurrent with the achievement of hemostasis, neutrophils are the first cells to migrate to the wound bed, brought in by pro-inflammatory signals including IL-8. Their apoptosis and engulfment by macrophages (efferocytosis) provides a key signal to the local immune milieu, including macrophages, to transition to an anti-inflammatory, pro-repair state, where angiogenesis occurs and granulation tissue is laid down. Myofibroblasts, activated through contractile forces and signaling molecules, then drive remodeling, where granulation tissue becomes scar. Unchecked inflammation at this stage can result in abnormal scar formation. SUMMARY: Although the derangement of immune signals at any stage can result in impaired wound healing, recent research has shown that the key transition point lies between the inflammatory and the proliferative phases. This review summarizes the events that facilitate this transition and discusses how this process can be disrupted, leading to chronic, non-healing wounds.
Overview
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Written from the paper’s full text.
TL;DR
This review summarizes immune mechanisms across hemostasis, inflammation, proliferation, and remodeling, arguing that the critical transition from the inflammatory to the proliferative phase often fails in chronic wounds. It highlights neutrophil apoptosis/efferocytosis and macrophage polarization as key drivers of repair.
Key findings
- Chronic wounds in the USA afflict approximately 6.5 million individuals and cost the healthcare system over 25 billion dollars annually; their mortality effect has been reported as comparable to cancer.
- Normal wound healing is divided into hemostasis (minutes to hours), inflammation (days 1–3), proliferation and repair (days 4–21), and remodeling (days 21–365); the key inflammatory-to-proliferative transition occurs around days 2–5 and often fails in chronic wounds.
- Neutrophils are early responders recruited by IL-8/CXCL8; their apoptosis and macrophage engulfment (efferocytosis) signal a shift to anti-inflammatory, pro-repair macrophages. Persistent neutrophils, NETs, proteases/MMPs, reactive oxygen species, and elevated CXCL8 contribute to chronic, non-healing wounds.
- Anti-inflammatory macrophages promote angiogenesis, granulation tissue, and re-epithelialization via VEGF, TGF-β, PDGF, EGF, KGF, and other signals; impaired pro- to anti-inflammatory macrophage transition—seen with iron overload, hyperglycemia, and hypoxia—stalls healing. Mature scars regain only 80% of initial tensile strength.
Methods
- Narrative review of the literature; no primary data, sample, or statistical analysis are reported.
- Synthesizes immune cell and signaling pathways across the four phases of wound healing, focusing on the inflammatory-to-proliferative transition and chronic wounds.
- Draws on cited animal models, in vitro studies, and human wound observations; no systematic search or meta-analysis is described.
Limitations
- The paper states no limitations.
- Evident from the text: it is a narrative review without systematic search, inclusion criteria, or quality appraisal.
- Evident from the text: many mechanistic conclusions rely on mouse models and in vitro findings, with limited direct human chronic wound data; no original experiments or quantitative synthesis are presented.
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Claims the paper makes
51 Not checked yet · 8 Own interpretation · 6 No basis given · 1 Partly supported · accuracy not yet measured
In the paper
“In impaired models of wound healing, such as diabetes, where infection risk is higher, neutrophils are clearly required [28].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [28] Wilgus TA, Roy S, McDaniel JC. Neutrophils and wound repair: positive actions and negative reactions. Adv Wound Care. 2013;2(7):379–88. https://doi.org/10.1089/wound.2012.0383 . source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Findings from mouse models of wound healing can be generalized to human wound healing and chronic wounds.
In the paper
“Their influx is mediated by a number of chemical signals, including IL-8, or CXCL8, as mentioned above, and neutrophils have over 30 different receptors that mitigate their migration and activation response [24].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [24] Futosi K, Fodor S, Mocsai A. Neutrophil cell surface receptors and their intracellular signal transduction pathways. Int Immunopharmacol. 2013;17(3):638–50. https://doi.org/10.1016/j.intimp.2013.06.034 . source
plaindirect- 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
“normal wound healing can generally be broken down into four over-lapping but distinct steps (Fig. 1). These steps include hemostasis (minutes to hours after injury), inflammation (days 1–3), proliferation and repair (days 4–21), and lastly, wound remodeling (days 21–365) [8, 9].”
§ Immunology of Wound Healing > Introduction
What the sources say
- Not checked yetcites [8] Morton LM, Phillips TJ. Wound healing and treating wounds: differential diagnosis and evaluation of chronic wounds. J Am Acad Dermatol. 2016;74(4):589–605; quiz −6. https://doi.org/10.1016/j.jaad.2015.08.068 . source
- Not checked yetcites [9] Reinke JM, Sorg H. Wound repair and regeneration. Eur Surg Res. 2012;49(1):35–43. https://doi.org/10.1159/000339613 . source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“chronic wounds demonstrate significantly increased levels of the potent neutrophil chemoattractant, CXCL8 [58].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [58] Fivenson DP, Faria DT, Nickoloff BJ, Poverini PJ, Kunkel S, Burdick M, et al. Chemokine and inflammatory cytokine changes during chronic wound healing. Wound Repair Regen. 1997;5(4):310–22. https://doi.org/10.1046/j.1524-475X.1997.50405.x . source
boostedcorrelational- 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
“Platelet activation not only results in hemostasis, but also in the release of growth factors such as platelet-derived growth factor (PDGF) as well as immune mediators that are responsible for activation of the immune system and transition to the inflammatory phase of wound healing.”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Hemostasis
plaindirect- 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
“mouse models of wound healing have shown that in non-aged, non-impaired models, neutrophil depletion does not negatively affect wound healing as profoundly as macrophage deletion [25–27].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [25] Leibovich SJ, Ross R. The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum. Am J Pathol. 1975;78(1):71–100.
- Not checked yetcites [26] Pinhal-Enfield G, Ramanathan M, Hasko G, Vogel SN, Salzman AL, Boons GJ, et al. An angiogenic switch in macrophages involving synergy between Toll-like receptors 2, 4, 7, and 9 and adenosine A(2A) receptors. Am J Pathol. 2003;163(2):711–21. https://doi.org/10.1016/s0002-9440(10)63698-x . source
- Not checked yetcites [27] Simpson DM, Ross R. The neutrophilic leukocyte in wound repair a study with antineutrophil serum. J Clin Invest. 1972;51(8):2009–23. https://doi.org/10.1172/jci107007 . source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Findings from mouse models of wound healing can be generalized to human wound healing and chronic wounds.
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
“New research has illustrated that chronic wounds fail to shift from the inflammatory to the proliferative phase of wound healing”
§ Immunology of Wound Healing > Introduction
boosted- 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
“recent research has shown that the key transition point lies between the inflammatory and the proliferative phases.”
- Also stated in: § Conclusions · plain
“Recent research has shown that the key transition point in wound healing lies between the inflammatory and the proliferative phases.”
§ Immunology of Wound Healing > Abstract > Summary
plain- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Conclusions · plain
None of the sources cited for this claim have been checked yet.
In the paper
“the immune system has been found to play a substantial role due to its impact on several repair mechanisms [6, 7].”
§ Immunology of Wound Healing > Introduction
What the sources say
- Not checked yetcites [6] MA S, MJ N. The innate immune system in acute and chronic wounds. Adv Wound Care. 2016;5(2):65–78. https://doi.org/10.1089/wound.2014.0608 . source
- Not checked yetcites [7] Strbo N, Yin N, Stojadinovic O. Innate and adaptive immune responses in wound epithelialization. Adv Wound Care. 2014;3(7):492–501. https://doi.org/10.1089/wound.2012.0435 . source
plaindirect- 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
“Myofibroblasts, activated through contractile forces and signaling molecules, then drive remodeling, where granulation tissue becomes scar.”
§ Immunology of Wound Healing > Abstract > Recent Findings
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
- It may state two separate claims as one. 15
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The inflammatory phase overlaps considerably with initial hemostasis, occurring during the first 72 h after tissue injury [16].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Partly supportedcites [16] Eming SA, Martin P, Tomic-Canic M. Wound repair and regeneration: mechanisms, signaling, and translation. Sci Transl Med. 2014;6(265):265sr6. https://doi.org/10.1126/scitranslmed.3009337 . sourceExperimental — accuracy not yet measured
The ‘Inflammatory response’ section says that acute wound-healing phases largely overlap and that the early inflammatory response occurs in parallel with hemostasis. It does not specify that the inflammatory phase occurs during the first 72 hours after injury; searches for that timing found no supporting passage in our copy. Page numbers were unavailable. (LLM, conf=0.85)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
- Partly supported
In the paper
“Concurrent with the achievement of hemostasis, neutrophils are the first cells to migrate to the wound bed, brought in by pro-inflammatory signals including IL-8.”
§ Immunology of Wound Healing > Abstract > Recent Findings
What the sources say
- Not checked yetcites [31] Baggiolini M, Loetscher P, Moser B. Interleukin-8 and the chemokine family. Int J Immunopharmacol. 1995;17(2):103–8. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Neutrophils represent the most abundant inflammatory cells to infiltrate a new wound and function mainly to remove debris and prevent infection [22, 23].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [22] Engelhardt E, Toksoy A, Goebeler M, Debus S, Brocker EB, Gillitzer R. Chemokines IL-8, GROalpha, MCP-1, IP-10, and Mig are sequentially and differentially expressed during phase-specific infiltration of leukocyte subsets in human wound healing. Am J Pathol. 1998;153(6):1849–60. source
- Not checked yetcites [23] de Oliveira S, Rosowski EE, Huttenlocher A. Neutrophil migration in infection and wound repair: going forward in reverse. Nat Rev Immunol. 2016;16(6):378–91. https://doi.org/10.1038/nri.2016.49 . source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“NETs have also been detected in excess in diabetic foot wounds and have been shown to delay healing, and inhibition of NETosis and NET function in mouse models of delayed wound healing improves outcomes [59•].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [59•]
plaindirect- 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Findings from mouse models of wound healing can be generalized to human wound healing and chronic wounds.
None of the sources cited for this claim have been checked yet.
In the paper
“Macrophages play a critical role in wound healing, and their roles in angiogenesis, fibroplasia, cell proliferation, and transition out of the inflammatory phase is clear (Fig. 2) [25–27, 60].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [25] Leibovich SJ, Ross R. The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum. Am J Pathol. 1975;78(1):71–100.
- Not checked yetcites [26] Pinhal-Enfield G, Ramanathan M, Hasko G, Vogel SN, Salzman AL, Boons GJ, et al. An angiogenic switch in macrophages involving synergy between Toll-like receptors 2, 4, 7, and 9 and adenosine A(2A) receptors. Am J Pathol. 2003;163(2):711–21. https://doi.org/10.1016/s0002-9440(10)63698-x . source
- Not checked yetcites [27] Simpson DM, Ross R. The neutrophilic leukocyte in wound repair a study with antineutrophil serum. J Clin Invest. 1972;51(8):2009–23. https://doi.org/10.1172/jci107007 . source
- Not checked yetcites [60] Koh TJ, DiPietro LA. Inflammation and wound healing: the role of the macrophage. Expert Rev Mol Med. 2011;13:e23. https://doi.org/10.1017/s1462399411001943 . source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“After hemostasis is achieved, histamine released by the activated complement cascade causes capillary dilation and leakage, accelerating migration of inflammatory cells into the wound bed and full transition to the inflammatory phase of wound healing [15].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Hemostasis
What the sources say
- Not checked yetcites [15] Sinno H, Prakash S. Complements and the wound healing cascade: an updated review. Plast Surg Int. 2013;2013:146764–7. https://doi.org/10.1155/2013/146764 . source
plaindirect- 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
“neutrophil-derived proteases, such as elastase and matrix metalloproteinases (MMPs), can degrade healthy extracellular matrix (ECM), and increased levels of these proteases have been repeatedly detected in chronic wounds [52–56].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [52] Briggaman RA, Schechter NM, Fraki J, Lazarus GS. Degradation of the epidermal-dermal junction by proteolytic enzymes from human skin and human polymorphonuclear leukocytes. J Exp Med. 1984;160(4):1027–42. source
- Not checked yetcites [53] Grinnell F, Zhu M. Fibronectin degradation in chronic wounds depends on the relative levels of elastase, alpha1-proteinase inhibitor, and alpha2-macroglobulin. J Invest Dermatol. 1996;106(2):335–41. source
- Not checked yetcites [54] Herrick S, Ashcroft G, Ireland G, Horan M, McCollum C, Ferguson M. Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation. Lab Invest. 1997;77(3):281–8.
- Not checked yetcites [55] Nwomeh BC, Liang HX, Cohen IK, Yager DR. MMP-8 is the predominant collagenase in healing wounds and nonhealing ulcers. J Surg Res. 1999;81(2):189–95. https://doi.org/10.1006/jsre.1998.5495 . source
- Not checked yetcites [56] Pirila E, Korpi JT, Korkiamaki T, Jahkola T, Gutierrez-Fernandez A, Lopez-Otin C, et al. Collagenase-2 (MMP-8) and matrilysin-2 (MMP-26) expression in human wounds of different etiologies. Wound Repair Regen. 2007;15(1):47–57. https://doi.org/10.1111/j.1524-475X.2006.00184.x . source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Platelet degranulation also leads to the release of inflammatory mediators such as interleukin (IL)-8, or CXCL8 (a potent neutrophil chemoattractant), in addition to IL-1α, IL-1β, IL-6, and tumor necrosis factor (TNF)-α, and activates the complement cascade [9, 14].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Hemostasis
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Dysregulation of any of these events can result in delayed wound healing and the potential to form chronic ulcers and/or excessive scarring [10••].”
§ Immunology of Wound Healing > Introduction
What the sources say
- Not checked yetcites [10••]
plaindirect- 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
“Not only do anti-inflammatory, pro-repair macrophages produce VEGF, which promotes vessel sprouting, they also express two transmembrane proteins that have been shown to promote vascular anastomosis [80, 85, 86].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Proliferation
What the sources say
- Not checked yetcites [80] Brancato SK, Albina JE. Wound macrophages as key regulators of repair: origin, phenotype, and function. Am J Pathol. 2011;178(1):19–25. https://doi.org/10.1016/j.ajpath.2010.08.003 . source
- Not checked yetcites [85] Fantin A, Vieira JM, Gestri G, Denti L, Schwarz Q, Prykhozhij S, et al. Tissue macrophages act as cellular chaperones for vascular anastomosis downstream of VEGF-mediated endothelial tip cell induction. Blood. 2010;116(5):829–40. https://doi.org/10.1182/blood-2009-12-257832 . source
- Not checked yetcites [86] Affolter M, Zeller R, Caussinus E. Tissue remodelling through branching morphogenesis. Nat Rev Mol Cell Biol. 2009;10:831–42. https://doi.org/10.1038/nrm2797 . source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Wounds without IL-6 lack an appropriate inflammatory response and demonstrate stunted angiogenesis, collagen accumulation, and re-epithelialization [89].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Proliferation
What the sources say
- Not checked yetcites [89] Lin ZQ, Kondo T, Ishida Y, Takayasu T, Mukaida N. Essential involvement of IL-6 in the skin wound-healing process as evidenced by delayed wound healing in IL-6-deficient mice. J Leukoc Biol. 2003;73(6):713–21. source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“When the transition from a pro- to an anti-inflammatory macrophage phenotype is impaired, wound healing stalls in the inflammatory phase and a chronic wound results [10••].”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
What the sources say
- Not checked yetcites [10••]
plaindirect- 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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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
“Additional signals, such as hyperglycemia in the setting of diabetes, hypoxia in the setting of arterial or venous insufficiency, or secondary infection likely also contribute to the persistence of pro-inflammatory macrophages.”
§ Immunology of Wound Healing > Four Stages of Wound Healing > Inflammation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“If wounds fail to transition from the inflammatory phase, pro-inflammatory macrophages persist and non-healing wounds develop.”
§ Immunology of Wound Healing > Conclusions
plaindirect- 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.
- Based: passes — The paper gives a reason why it holds.
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
“Numerous signals are responsible for the transition, most notably the apoptosis and phagocytosis of wound-bed resident neutrophils (efferocytosis).”
§ Immunology of Wound Healing > Conclusions
plaindirect- Asserted: passes — The authors put it forward as true.
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- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
The paper relies on this without support.
Findings from mouse models of wound healing can be generalized to human wound healing and chronic wounds.
“mouse models of wound healing have shown that in non-aged, non-impaired models, neutrophil depletion does not negatively affect wound healing as profoundly as macrophage deletion [25–27].”
“in a mouse model of iron overload, local wound macrophages persisted in a pro-inflammatory state with excess production of inducible nitric oxide synthase (iNOS), IL-12, and TNF-α, in addition to free radicals, leading to impaired wound healing [81].”
“inhibition of NETosis and NET function in mouse models of delayed wound healing improves outcomes [59•].”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Immune regulators promote better surveillance and wound clearance in multiple tissues [75, 76].”
From Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin (2020) · cites this paper as [75]
Experimental — accuracy not yet measuredIn the citing paper
“Indeed, these cells are known to be irreplaceable partners in a successful wound healing70.”
From Platelets induce increased estrogen production through NF-κB and TGF-β1 signaling pathways in endometriotic stromal cells (2020) · cites this paper as [70]
In the citing paper
“The absence or over-abundance of any of these cell types would derail the normal healing process, leading healing astray and causing pathological healing such as fibrosis70.”
From Platelets induce increased estrogen production through NF-κB and TGF-β1 signaling pathways in endometriotic stromal cells (2020) · cites this paper as [70]
Citations
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Neutrophil Extracellular Traps Kill Bacteria
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Exploring the full spectrum of macrophage activation
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The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
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Metadata
- Authors
- Ellis, S., Lin, E. J., & Tartar, D.
- Affiliations
- University of California, Davis (US)
- Corresponding author
- Tartar, Danielle
- ORCID
- Tartar, Danielle
- Venue
- Current Dermatology Reports
- Published
- 2018-09-28
- Volume
- 7
- Issue
- 4
- Pages
- 350-358
- ISSN
- 2162-4933 (ISSN-L)
- PMC
- PMC6244748
- OpenAlex
- W2892642834
- Semantic Scholar
- 2db5782e12aeaff45400ab4236b744f21a3178e0
- Cited by
- 625
- References
- 105
- Citations by year
- 2026: 65 · 2025: 114 · 2024: 109 · 2023: 90 · 2022: 96 · 2021: 86 · 2020: 44 · 2019: 21
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Current Dermatology Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Health Sciences › Medicine › Dermatology › Dermatologic Treatments and Research
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- wound healing, chronic wounds, skin wound healing, neutrophils, efferocytosis, macrophages, interleukin-8, inflammation, angiogenesis, granulation tissue, myofibroblasts, scar formation, keratinocytes, dermal cells, immune signaling
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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