Cellular resolution of inflammation—catabasis
Abstract
Controlled inflammation has become a central focus in chronic disease therapeutics. Exaggerated inflammation is a common factor that contributes to matrix destruction, cellular senescence, and nonhealing in a variety of disease processes. Efforts at controlling inflammation have traditionally concentrated on systemic antagonists to inflammation such as nonsteroidal anti‐inflammatory agents. More recently, following increased appreciation of local biological cellular and molecular events occurring at the wound interface, efforts are being focused on local targeted approaches to catabasis, the resolution of inflammation. These efforts relate to the isolation and understanding of the mechanisms of actions of various “stop signal mediators.” These lipoxins, resolvins, and protectins are produced and stimulated by cellular interactions in the blood stream, extracellular matrix, and in cells themselves. Transmission of these signals between cells and the extracellular matrix and between cells themselves occurs via a variety of mechanisms including through intracellular gap junctions, connexins, and cadherins. The existence of these mediators, signals, and channels of communication all provide new therapeutic options for achieving catabasis in a more defined and targeted fashion.
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Apoptosis and engulfment of neutrophils by macrophages provides a key signal to the local immune milieu to transition to an anti-inflammatory, pro-repair state.
“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”
From Immunology of Wound Healing (2018) · cites this paper as [49]
In physiologic wound repair, neutrophil apoptosis followed by local macrophage uptake of apoptotic neutrophils triggers a transition out of the inflammatory phase.
“In physiologic wound repair, neutrophils undergo apoptosis after carrying out their various functions at the site of injury. Local macrophage uptake of apoptotic neutrophils then triggers a transition out of inflammatory phase [47–49].”
From Immunology of Wound Healing (2018) · cites this paper as [49]
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- Authors
- Widgerow, A. D.
- Affiliations
- University of the Witwatersrand (ZA)
- Corresponding author
- Widgerow, Alan D.
- ORCID
- Widgerow, Alan D.
- Venue
- Wound Repair and Regeneration
- Publisher
- Wiley
- Published
- 2012-01
- Volume
- 20
- Issue
- 1
- Pages
- 2-7
- ISSN
- 1067-1927 (ISSN-L)
- 1524-475X
- OpenAlex
- W1935740361
- Cited by
- 48
- References
- 28
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 5 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 4
- FWCI
- 3.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Wound Repair and Regeneration (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Keywords
- inflammation resolution, katabasis, lipoxins, resolvins, protectins, gap junctions, connexins, cadherins, extracellular matrix, cellular senescence, wound healing, chronic wounds
- MeSH terms
- Cell Communication, Docosahexaenoic Acids, Humans, Inflammation, Wound Healing, Wounds and Injuries, Inflammation Mediators, CD59 Antigens, Lipoxins, Complement Inactivating Agents
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