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Cell migration inducing hyaluronidase 2 (CEMIP2) is a type II transmembrane protein functioning as a cell surface hyaluronidase, highly specific for hyaluronan, which it cleaves from high molecular weight forms to intermediate-sized fragments[1][3][5]. This enzyme is critical for extracellular matrix remodeling, regulating cell adhesion and migration, and influencing angiogenesis, as well as heart and skeletal morphogenesis[1]. CEMIP2 participates importantly in the catabolism and turnover of systemic hyaluronan and is implicated in the pathological progression of cancer and fibrotic processes[2]. It is also essential for normal hearing, as loss-of-function mutations are linked to non-syndromic hearing loss[1]. It may have additional roles in immune responses, especially antiviral defenses via activation of the JAK/STAT pathway[1]. Modulation of CEMIP2, including experimental inhibition by compounds such as ipriflavone, is under investigation for potential therapeutic or diagnostic uses in various diseases, particularly cancer, fibrosis, and inflammatory conditions[2].
Hyaluronidase inhibition (ipriflavone): decreases HA degradation, lowers ECM remodeling and MMPs expression; Potential modulation of JAK/STAT and Wnt/β-catenin pathways by targeting CEMIP2
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