The Role of Transient Receptor Potential Canonical 3 (TRPC3) in Wound Healing

ABSTRACT Wound healing is a complex, highly orchestrated process involving distinct yet overlapping phases: hemostasis, inflammation, proliferation, and remodeling. Effective healing requires precise cellular and molecular interactions across these phases, with calcium signaling playing a pivotal role in modulating cellular responses such as migration, proliferation, and differentiation. Among the calcium channels involved, the Transient Receptor Potential Canonical (TRPC) family, particularly TRPC3, emerged as a key modulator of wound repair processes. In this review, we explore the dynamic contributions of TRPC3 to each phase of wound healing, highlighting its regulation of calcium fluxes and the downstream cellular responses critical for effective tissue repair. We will further discuss the altered role of TRPC3 in pathological conditions, such as chronic wounds and diabetic ulcers, where aberrant TRPC3 signaling disrupts normal wound healing, contributing to impaired resolution and fibrosis. By summarizing findings from recent studies, we underscore the potential of targeting TRPC3 as a therapeutic strategy to restore normal wound healing. Finally, we will discuss future directions in TRPC3‐targeted interventions, including the development of selective modulators and the use of TRPC3‐targeting therapy, to address unmet needs in wound care. This review aims to provide a comprehensive overview of TRPC3's multifaceted role in wound repair and its therapeutic potential in regenerative medicine.