Background: Beta-catenin has been historically recognized as both an intermediate in the "canonical Wnt signaling pathway" and as a component of functional adherens junctions.
Materials and methods: Cellular accumulation of beta-catenin levels can result in transactivation of gene transcription and cellular proliferation during normal cellular and disease development. Recent evidence has identified beta-catenin in an additional role as a component of cutaneous wound healing.
Results: This finding is in keeping with previous observations that post-translational modifications of beta-catenin that are associated with its cytoplasmic accumulation are frequently observed in fibroproliferative diseases with characteristics of dysregulated wound healing. These diseases include hypertrophic scar formation, aggressive fibromatoses, Lederhose disease, and Dupuytren's contracture (DC).
Conclusions: While its precise roles in disease initiation and progression remain to be explored, this review highlights our current knowledge of beta-catenin regulation and describes some potential upstream mediators of beta-catenin accumulation and signaling in fibroproliferative disease.