Toll-like receptors, wound healing, and carcinogenesis

Following acute injury, the concerted action of resident and nonresident cell populations evokes wound healing responses that entail a temporary increase in inflammation, extracellular matrix production, and proliferation to ultimately restore normal organ architecture. However, chronic injury evoke...

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Bibliographic Details
Published in:Journal of molecular medicine (Berlin, Germany) Germany), 2009-02, Vol.87 (2), p.125-138
Main Authors: Kluwe, Johannes, Mencin, Ali, Schwabe, Robert F.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cell Transformation, Neoplastic
General aspects
Human Genetics
Humans
Inflammation - physiopathology
Internal Medicine
Medical sciences
Models, Biological
Molecular Medicine
Neoplasms - physiopathology
Review
Signal Transduction - physiology
Toll-Like Receptors - physiology
Wound Healing - physiology
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Summary:Following acute injury, the concerted action of resident and nonresident cell populations evokes wound healing responses that entail a temporary increase in inflammation, extracellular matrix production, and proliferation to ultimately restore normal organ architecture. However, chronic injury evokes a perpetuating wound healing response promoting the development of fibrosis, organ failure, and cancer. Recent evidence points toward toll-like receptors (TLRs) as important regulators of inflammatory signals in wound healing. Here, we will review the activation of TLRs by different endogenous and bacterial TLR ligands during wound healing, and the contribution of TLR-induced signals to injury, fibrogenesis, regeneration, and carcinogenesis. We will discuss the hypothesis that TLRs act as sensors of danger signals in injured tissue to switch the wound healing response toward fibrogenesis and regeneration as a protective response to imminent danger at the cost of an increased long-term risk of developing scars and cancer.
ISSN:0946-2716
1432-1440
DOI:10.1007/s00109-008-0426-z