The adverse physiological and psychological effects of scars are broad, and there are currently no reliable treatments to prevent scarring. In contrast to adult wounds, early gestation fetal skin wounds repair rapidly and in the absence of scar formation. This intrinsic ability of fetal skin requires biochemical signals, which start at the cellular level and lead to secretion of transforming factors and expression of receptors, and specific markers that promote wound healing without scar formation. Despite extensive investigation, the mechanisms and molecular pathways of wound healing still need to be elucidated to achieve a complete understanding of this remodeling system. For some time, it has been known that significant differences exist among the extracellular matrix, inflammatory response, cellular mediators, and gene expression profiles of fetal and postnatal wounds. The aim of this paper is to discuss the main molecular markers involved in scarless skin wound healing, their respective mechanisms of action as well as problems and perspectives of scarring treatment.