This study found that type XVII collagen (COL17) regulates interfollicular epidermis proliferation in both neonatal and aged mice through Wnt signaling, suggesting its potential as a target for anti-aging skin strategies.
124 citations
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July 2017 in “eLife” This study found that COL17 deficiency in neonatal mice causes abnormal skin cell proliferation due to disrupted Wnt signaling, while replenishing or overexpressing COL17 can reverse this effect in both neonatal and aged skin.
This study found that in mice, type XVII collagen is essential for controlling epidermal cell proliferation through Wnt signaling, with its deficiency or altered distribution leading to skin hyperproliferation and aging-like changes.
September 2016 in “Journal of dermatological science” This study found that COL17 plays a key role in regulating epidermal keratinocyte differentiation and proliferation, influencing the expression of differentiation markers and cellular growth in specific conditions.
63 citations
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March 2018 in “Experimental Dermatology” This review explores the physiological roles of collagen XVII in the epidermis, its involvement in stem cell maintenance, and its connections with signaling pathways, but it reports no new results.