Mechanisms of Peritoneal Mesothelial Cells in Peritoneal Adhesion

Abstract

A peritoneal adhesion (PA) is a fibrotic tissue connecting the abdominal or visceral organs to the peritoneum. The formation of PAs can induce a variety of clinical diseases. However, there is currently no effective strategy for the prevention and treatment of PAs. Damage to peritoneal mesothelial cells (PMCs) is believed to cause PAs by promoting inflammation, fibrin deposition, and fibrosis formation. In the early stages of PA formation, PMCs undergo mesothelial-mesenchymal transition and have the ability to produce an extracellular matrix. The PMCs may transdifferentiate into myofibroblasts and accelerate the formation of PAs. Therefore, the aim of this review was to understand the mechanism of action of PMCs in PAs, and to offer a theoretical foundation for the treatment and prevention of PAs.

Keywords: fibrosis; inflammation; mesothelial–mesenchymal transition; peritoneal adhesions; peritoneal mesothelial cells.

Figure 1

(A) Early stage of peritoneal adhesion (PA) formation: peritoneal mesothelial cells (PMCs) undergo shedding, necrosis, and phenotypic changes, form membrane protrusions, and fuse with each other to form early adhesions in the stimulated environment. (B) Intermediate stage of PA formation: PMCs initiate inflammatory responses by secreting inflammatory factors, adhesion molecules, and pro-fibrotic factors. Moreover, they are affected by the inflammatory environment, which stimulates them to further exacerbate the inflammatory process. At the same time, the fibrinolytic system is dysfunctional, causing excessive deposition of fibrin. (C) Late stage of PA formation: PMCs undergo mesothelial–mesenchymal transition (MMT) to form myofibroblasts. (D) Late stage of PA formation: myofibroblasts secrete a large amount of extracellular matrix to finally form a PA.