The pathophysiology underlying the formation, progression, and surgical healing of incisional hernia (IH) that develops as a major complication associated with abdominal laparotomy is poorly understood. The proposed mechanisms include the switch of collagen phenotype and the proliferation of abnormal fibroblasts after surgery. The focus of this article was to critically review the cellular, biochemical, and potential molecular events associated with the development of IH. The disturbance in collagen homeostasis with alterations in the expression of collagen subtypes, including type 1, type 3, type 4, and type 5, and impairment in the transdifferentiation of fibroblasts to myofibroblasts are discussed. The phenotype switch of wound-repair fibroblasts results in mechanically compromised extracellular matrix that triggers the proliferation of abnormal fibroblasts. High-mobility group box 1 could be involved in wound progression, whereas signaling events mediated by tumor necrosis factor β1, connective tissue growth factor, lysyl oxidase, and hypoxia-inducible factor 1 play significant role in the wound healing response. Thus, the ratio of tumor necrosis factorβ1: high-mobility group box 1 could be a critical determinant of the underlying pathology. Potential target sites for therapeutic intervention in the management of IH are recognized.
Keywords: Collagen phenotypes; Incisional hernia; Matrix homeostasis; Myofibroblasts; TGF-β1 signaling.
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