Search

Keloids, fibroproliferative dermal tumors with effusive accumulation of extracellular matrix (ECM) components, particularly collagen, result from excessive expression of growth factors and cytokines. The etiology of keloids is unknown but they occur after dermal injury in genetically susceptible individuals, and they cause both physical and psychological distress for the affected individuals. Several treatment methods for keloids exist, including the combination therapy of surgical excision followed by intralesional steroid therapy, however, they have high recurrence rate regardless of the current treatment method. Improved understanding of the pathomechanisms leading to keloid formation will hopefully identify pathways that serve as specific targets to improve therapy for this devastating, currently intractable, disorder. [ABSTRACT FROM AUTHOR]

Animal models are crucial for the study of fibrosis. Keloids represent a unique type of fibrotic scarring that occurs only in humans, thus presenting a challenge for those studying the pathogenesis of this disease and its therapeutic options. Here, several animal models of fibrosis currently in use are described, emphasizing recent progress and highlighting encouraging challenges. [ABSTRACT FROM AUTHOR]

The article presents a study related to role of cellular fibronectin in keloid. Topics discussed include presence of finbronbectin protein in extracellular matrix, the human fibronectin (FN) gene, encoding of an extra domain A (EDA) an alternative spliced exon, findings inferring role of FN-EDA in wound healing and fibroproliferative disorders and possibilities of disrupting fibrotic reaction in keloids by preventing synthesis or interactions of FN-EDA.