T
Thomas Krieg
Researcher at University of Cologne
Publications - 310
Citations - 27878
Thomas Krieg is an academic researcher from University of Cologne. The author has contributed to research in topics: Extracellular matrix & Fibroblast. The author has an hindex of 76, co-authored 299 publications receiving 25798 citations. Previous affiliations of Thomas Krieg include German Cancer Research Center & Max Planck Society.
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Journal Article
Scleroderma (systemic sclerosis): classification, subsets and pathogenesis.
LeRoy Ec,Carol M. Black,Fleischmajer R,Jablonska S,Thomas Krieg,Thomas A. Medsger,N R Rowell,Frank A. Wollheim +7 more
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Inflammation in wound repair: molecular and cellular mechanisms.
TL;DR: Cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair are reviewed and a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response is provided.
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Keratinocyte–Fibroblast Interactions in Wound Healing
TL;DR: This review focuses on the role of keratinocyte-fibroblast interactions in the wound-healing process and the phenotype of fibroblasts from different tissues or body sites becomes better defined, so as to understand their individual contribution in wound healing in more detail and possibly explain different clinical outcomes.
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Differential Roles of Macrophages in Diverse Phases of Skin Repair
Tina Lucas,Ari Waisman,Rajeev Ranjan,Jürgen Roes,Thomas Krieg,Werner Müller,Axel Roers,Sabine A. Eming +7 more
TL;DR: The results demonstrate that macrophages exert distinct functions during the diverse phases of skin repair, which are crucial to control the natural sequence of repair events.
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The function of KGF in morphogenesis of epithelium and reepithelialization of wounds
Sabine Werner,Hans Smola,Xiang Liao,Michael T. Longaker,Thomas Krieg,Peter Hans Hofschneider,Lewis T. Williams +6 more
TL;DR: Upon skin injury, inhibition of KGF receptor signaling reduced the proliferation rate of epidermal keratinocytes at the wound edge, resulting in substantially delayed reepithelialization of the wound.