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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, Jahrgang 87, Nr. 2, 2, 2009, S. 125-138.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kluwe, J, Mencin, A & Schwabe, RF 2009, 'Toll-like receptors, wound healing, and carcinogenesis.', J MOL MED, Jg. 87, Nr. 2, 2, S. 125-138. <http://www.ncbi.nlm.nih.gov/pubmed/19089397?dopt=Citation>

APA

Kluwe, J., Mencin, A., & Schwabe, R. F. (2009). Toll-like receptors, wound healing, and carcinogenesis. J MOL MED, 87(2), 125-138. [2]. http://www.ncbi.nlm.nih.gov/pubmed/19089397?dopt=Citation

Vancouver

Kluwe J, Mencin A, Schwabe RF. Toll-like receptors, wound healing, and carcinogenesis. J MOL MED. 2009;87(2):125-138. 2.

Bibtex

@article{d60109690dc34f87a6648889d9d02c39,
title = "Toll-like receptors, wound healing, and carcinogenesis.",
abstract = "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.",
keywords = "Animals, Humans, Cell Transformation, Neoplastic, Inflammation physiopathology, Models, Biological, Neoplasms physiopathology, Signal Transduction physiology, Toll-Like Receptors physiology, Wound Healing physiology, Animals, Humans, Cell Transformation, Neoplastic, Inflammation physiopathology, Models, Biological, Neoplasms physiopathology, Signal Transduction physiology, Toll-Like Receptors physiology, Wound Healing physiology",
author = "Johannes Kluwe and Ali Mencin and Schwabe, {Robert F}",
year = "2009",
language = "Deutsch",
volume = "87",
pages = "125--138",
journal = "J MOL MED",
issn = "0946-2716",
publisher = "Springer",
number = "2",

}

RIS

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 -