Molecular and cellular aspects of the pathogenesis of incisional hernias

The incisional hernias are one of the most common surgical pathologies worldwide. The achievements of medical science in recent decades have significantly improved the results of treatment of this disease, due to the justification and implementation of various methods of hernioplasty with implantation of synthetic endoprostheses. At the same time, the incidence rate of incisional hernias remains fairly high. For several years, research has been conducted to study the molecular and cellular mechanisms of incisional hernias formation. The key issue in the problem of tissue repair disorders after laparotomy is to understand the processes of extracellular matrix organization and fibroblast activation. The extracellular matrix appears to be a unique environment that promotes the proper structuring of collagen fibers, the acquisition of postoperative scar strength and timely wound cavity contraction. The regulation of extracellular matrix homeostasis depends on many factors that affect the timing and usefulness of tissue repair after surgical trauma. The main regenerative potential consists of populations of fibroblasts responsible for the synthesis and degradation of collagen. Extracellular matrix and fibroblasts have a multifactorial effect on wound repair and imbalance of their interaction can contribute to the formation of incisional hernias. Molecular compounds synthesized by fibroblasts, which include matrix metalloproteinases, matrix metalloproteinase inhibitors, as well as actin and collagen proteins, play an important role both in the healing of surgical wounds and in the formation of hernias. Identification of critical points in the pathogenesis of incisional hernias at the molecular and cellular levels will make it possible to predict and prevent their formation. This opens up new opportunities for precision stratification of patients before abdominal wall hernia repair and the choice of personalized surgical tactics.