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عمومی::
اپیتلیالیزاسیون، اپیتلیالیزاسیون
(2014) found that apoptosis of skin- resident macrophages activated epithelial hair follicle stem cells, which contribute to hair regeneration (Castellana et al.
ASK1 has previously been shown to be increased in the epithelial layer of wound peripheries in rats (Funato et al.
The specific role of Langerhans cells in wound healing-particularly chronic-has yet to be defined, however, they do repopulate the epidermis during re- epithelialization in acute wound models (Stojadinovic et al.
These treatments resulted in wound closure and re- epithelialization while control wounds treated with a non-specific antibody remained unhealed with scabs.
Disturbances in macrophage function can lead to aberrant repair, such that uncontrolled production of in- flammatory mediators and growth factors, deficient generation of anti-inflammatory macrophages, or failed communication between macrophages and epithelial cells, endothelial cells, fibroblasts, and stem or tissue progenitor cells all contribute to a state of persistent injury, and this could lead to the development of path- ological fibrosis.،(2014) found that apoptosis of skin- resident macrophages activated epithelial hair follicle stem cells, which contribute to hair regeneration (Castellana et al.
ASK1 has previously been shown to be increased in the epithelial layer of wound peripheries in rats (Funato et al.
The specific role of Langerhans cells in wound healing-particularly chronic-has yet to be defined, however, they do repopulate the epidermis during re- epithelialization in acute wound models (Stojadinovic et al.
These treatments resulted in wound closure and re- epithelialization while control wounds treated with a non-specific antibody remained unhealed with scabs.
Disturbances in macrophage function can lead to aberrant repair, such that uncontrolled production of in- flammatory mediators and growth factors, deficient generation of anti-inflammatory macrophages, or failed communication between macrophages and epithelial cells, endothelial cells, fibroblasts, and stem or tissue progenitor cells all contribute to a state of persistent injury, and this could lead to the development of path- ological fibrosis.
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