Rima Patel, Lily Waltz, Gemma Toogood, Wei Li, Junwang Xu
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引用次数: 0
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.
期刊介绍：
The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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