دورية أكاديمية

Exploiting PI3 K/m TOR signaling to accelerate epithelial wound healing.

التفاصيل البيبلوغرافية
العنوان: Exploiting PI3 K/m TOR signaling to accelerate epithelial wound healing.
المؤلفون: Castilho, RM, Squarize, CH, Gutkind, JS
المصدر: Oral Diseases; Sep2013, Vol. 19 Issue 6, p551-558, 8p, 4 Color Photographs
مصطلحات موضوعية: EPIDERMIS, TUBEROUS sclerosis, EPITHELIUM, CELLULAR signal transduction, GENES, HOMEOSTASIS, PROTEINS, SKIN physiology, WOUND healing, GENETICS, WOUNDS & injuries, PHYSIOLOGY
مستخلص: The molecular circuitries controlling the process of skin wound healing have gained new significant insights in recent years. This knowledge is built on landmark studies on skin embryogenesis, maturation, and differentiation. Furthermore, the identification, characterization, and elucidation of the biological roles of adult skin epithelial stem cells and their influence in tissue homeostasis have provided the foundation for the overall understanding of the process of skin wound healing and tissue repair. Among numerous signaling pathways associated with epithelial functions, the PI3 K/ Akt/m TOR signaling route has gained substantial attention with the generation of animal models capable of dissecting individual components of the pathway, thereby providing a novel insight into the molecular framework underlying skin homeostasis and tissue regeneration. In this review, we focus on recent findings regarding the mechanisms involved in wound healing associated with the upregulation of the activity of the PI3 K/ Akt/m TOR circuitry. This review highlights critical findings on the molecular mechanisms controlling the activation of mTOR, a downstream component of the PI3 K- PTEN pathway, which is directly involved in epithelial migration and proliferation. We discuss how this emerging information can be exploited for the development of novel pharmacological intervention strategies to accelerate the healing of critical size wounds. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:1354523X
DOI:10.1111/odi.12070