Toll-like receptors, wound healing, and carcinogenesis.
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Toll-like receptors, wound healing, and carcinogenesis. / Kluwe, Johannes; Mencin, Ali; Schwabe, Robert F.
In: J MOL MED, Vol. 87, No. 2, 2, 2009, p. 125-138.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Toll-like receptors, wound healing, and carcinogenesis.
AU - Kluwe, Johannes
AU - Mencin, Ali
AU - Schwabe, Robert F
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Animals
KW - Humans
KW - Cell Transformation, Neoplastic
KW - Inflammation physiopathology
KW - Models, Biological
KW - Neoplasms physiopathology
KW - Signal Transduction physiology
KW - Toll-Like Receptors physiology
KW - Wound Healing physiology
KW - Animals
KW - Humans
KW - Cell Transformation, Neoplastic
KW - Inflammation physiopathology
KW - Models, Biological
KW - Neoplasms physiopathology
KW - Signal Transduction physiology
KW - Toll-Like Receptors physiology
KW - Wound Healing physiology
M3 - SCORING: Zeitschriftenaufsatz
VL - 87
SP - 125
EP - 138
JO - J MOL MED
JF - J MOL MED
SN - 0946-2716
IS - 2
M1 - 2
ER -