Inflammation in Wound Repair: Molecular and Cellular Mechanisms
Open accessAbstract
In post-natal life the inflammatory response is an inevitable consequence of tissue injury. Experimental studies established the dogma that inflammation is essential to the establishment of cutaneous homeostasis following injury, and in recent years information about specific subsets of inflammatory cell lineages and the cytokine network orchestrating inflammation associated with tissue repair has increased. Recently, this dogma has been challenged, and reports have raised questions on the validity of the essential prerequisite of inflammation for efficient tissue repair. Indeed, in experimental models of repair, inflammation has been shown to delay healing and to result in increased scarring. Furthermore, chronic inflammation, a hallmark of the non-healing wound, predisposes tissue to cancer development. Thus, a more detailed understanding in mechanisms controlling the inflammatory response during repair and how inflammation directs the outcome of the healing process will serve as a significant milestone in the therapy of pathological tissue repair. In this paper, we review cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair and provide a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response.
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We know much less about how inflammation is resolved during normal wound healing than about initiation and amplification, which is prerequisite for understanding pathogenesis of persistent inflammation in chronic wounds.
“Compared with the process of initiation and amplification of the inflammatory response, we know much less about how inflammation is resolved during normal wound healing, which is prerequisite for understanding the pathogenesis of persistent inflammation in chronic wounds [6].”
From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [6]
Persisting inflammatory cells generate proinflammatory cytokines and a highly proteolytic microenvironment at the wound site.
“Persisting inflammatory cells, mainly neutrophils and macrophages, generate large amount of proinflammatory cytokines and a highly proteolytic microenvironment at the wound site [6].”
From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [6]
Early fetal wounds have minimal inflammation and exhibit scarless regeneration, whereas provoked inflammation in fetal wounds exacerbates scar formation.
“For example, the early fetal wound has minimal inflammation and exhibits scarless regeneration, whereas scar formation is exacerbated when inflammation is provoked in fetal wounds [6].”
From Transition from inflammation to proliferation: a critical step during wound healing (2016) · cites this paper as [6]
Excessive ECM deposition by myofibroblasts can lead to fibrosis, scarring, and loss of tissue function if not kept in check.
“However, if ECM synthesis in myofibroblasts is not kept in check, then excessive matrix deposition can lead to fibrosis, scarring, and loss of tissue function [120–122].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [122]
Macrophages are the main source of cytokines and growth factors stimulating fibroblast proliferation and collagen biosynthesis.
“they are the main source of cytokines and growth factors stimulating the proliferation of fibroblasts and collagen biosynthesis [3, 36, 57–59].”
From The role of the extracellular matrix components in cutaneous wound healing (2014) · cites this paper as [57]
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- Authors
- Eming, S. A., Krieg, T., & Davidson, J. M.
- Affiliations
- University of Cologne (DE)
- Vanderbilt University (US)
- Corresponding author
- Eming, Sabine A.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2007-03
- Volume
- 127
- Issue
- 3
- Pages
- 514-525
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W2041591721
- Cited by
- 2,429
- References
- 130
- Citations by year
- 2026: 154 · 2025: 198 · 2024: 168 · 2023: 145 · 2022: 200 · 2021: 155 · 2020: 149 · 2019: 135 · 2018: 134 · 2017: 129 · 2016: 149 · 2015: 144 · 2014: 132 · 2013: 102 · 2012: 88
- FWCI
- 6.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r15ar044104-01)
- National Institute on Aging (AG-06528, R01AG006528)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-44104)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- inflammation, wound healing, chronic inflammation, chronic wounds, scar formation, cytokine network, cancer susceptibility, inflammation modulation
- MeSH terms
- Animals, Cells, Cultured, Fibroblasts, Humans, Inflammation, Models, Biological, Neoplasms, Phenotype, Skin, Wound Healing, Keratinocytes, Mice
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