Interaction of the AKT and β-catenin signalling pathways and the influence of photobiomodulation on cellular signalling proteins in diabetic wound healing

The induction of a cells destiny is a tightly controlled process that is regulated through communication between the matrix and cell signalling proteins. Cell signalling activates distinctive subsections of target genes, and different signalling pathways may be used repeatedly in different settings. A range of different signalling pathways are activated during the wound healing process, and dysregulated cellular signalling may lead to reduced cell function and the development of chronic wounds. Diabetic wounds are chronic and are characterised by the inability of skin cells to act in response to reparative inducements. Serine/threonine kinase, protein kinase B or AKT (PKB/ AKT), is a central connection in cell signalling induced by growth factors, cytokines and other cellular inducements, and is one of the critical pathways that regulate cellular proliferation, survival, and quiescence. AKT interacts with a variety of other pathway proteins including glycogen synthase kinase 3 beta (GSK3 beta) and beta-catenin. Novel methodologies based on comprehensive knowledge of activated signalling pathways and their interaction during normal or chronic wound healing can facilitate quicker and efficient diabetic wound healing. In this review, we focus on interaction of the AKT and beta-catenin signalling pathways and the influence of photobiomodulation on cellular signalling proteins in diabetic wound healing.