Ectodysplasin A2 receptor (EDA2R)

Ectodysplasin A2 receptor (EDA2R, also known as XEDAR, TNFRSF27) is a type III transmembrane protein in the tumor necrosis factor receptor superfamily that binds specifically to the EDA-A2 isoform of ectodysplasin A, but not EDA-A1[3][5]. This receptor plays key roles in developmental and pathological processes, including the regulation of hair follicle cycling, teeth formation, and skeletal muscle homeostasis, as well as modulating apoptosis and inflammatory responses via activation of NF-κB and JNK signaling[1][2][3]. EDA2R is upregulated in conditions of aging, metabolic disorders, and several diseases such as androgenetic alopecia, diabetic nephropathy, and cancer[1][2][3]. Its expression is both a marker and a potential mediator of tissue aging and inflammation, with emerging evidence highlighting it as a promising—but as yet untargeted—therapeutic receptor for interventions in age-associated and inflammatory disorders[1].

Other names

Tumor necrosis factor receptor superfamily member 27TNFRSF27X-linked ectodermal dysplasia receptorXEDAREDA-A2 receptorEDA-A2REDAA2R

No drugs currently established; theoretical mechanisms involve antagonizing EDA2R/EDA-A2 interaction to inhibit downstream NF-κB and MAPK pathway activation