Peritoneal adhesions (PAs) are abnormal fibrous bands between damaged tissues and organs in the abdominal cavity caused by surgery, peritoneal inflammation, peritoneal dialysis, etc. Among them, surgery is the leading cause of PAs. PAs can cause infertility, intestinal obstruction, intestinal perforation, and other clinical complications. Secondary adhesiolysis surgery is the primary treatment option, but it is prone to recurrence and has various complications and risks. In recent years, a series of drugs and barrier materials have been developed to prevent and treat PAs, but the effect is not satisfactory. PA-resistant drugs increase the risk of bleeding and inhibit normal immune function. Although barrier materials can alleviate the progress of PAs to a certain extent, they cannot achieve the ideal effect of anti-PAs because they cannot cover the peritoneal injury site for a long time, and the degradation is not complete. Therefore, breakthroughs are needed in the prevention and treatment of PAs. Recent studies have shown that PAs result from various events, including vascular injury, platelet aggregation, coagulation cascade, and fibrin deposition. Eventually, fibrin and extracellular matrix deposition form adhesion bands and later develop contractile scarring and cause clinical symptoms. In the above events, various cells involved in PAs play a crucial role. Peritoneal mesothelial cells (PMCs), neutrophils, eosinophils, T lymphocytes, macrophages, mast cells, etc., are distributed in the peritoneal microenvironment. Under physiological conditions, these cellular components are significant for the dynamic stabilization of the peritoneal microenvironment. When bacteria and foreign bodies invade the peritoneal cavity, fibrin and inflammatory cells exude with the peritoneal fluid to limit, remove, and absorb foreign bodies. Finally, the fibrin is absorbed, and the peritoneal injury usually heals. Under pathological conditions, the above cells are dysfunctional, promoting the progression of PAs. Dysfunction of PMC function promotes initial PA formation, expanded inflammatory response, and excessive fibrin deposition; neutrophils and peritoneal resident macrophages are first recruited to the peritoneal injury site, the former mediates the inflammatory response, and the latter covers the injury site for a transient protective effect; intermediate and advanced neutrophils of PAs form neutrophil extracellular traps and synergize with other cells to promote fibrosis progression and lead to PA formation. Here, the authors review the action mechanisms of various cells in the peritoneal microenvironment in the pathogenesis and development of PAs and the connections and interactions of multiple cells in the progression of PAs. In addition, the main measures for the prevention and treatment of PAs, which have been widely studied in recent years are introduced, and the prevention and treatment strategies focused on the cells involved in PAs are summarized, hoping to provide new ideas for the clinical prevention and treatment of PAs.