Abstract
Formation of peritoneal adhesions (PA) is one of the major complications following intra-abdominal surgery. It is primarily caused by activation of the mesothelial layer and underlying tissues in the peritoneal membrane resulting in the transition of mesothelial cells (MCs) and fibroblasts to a pro-fibrotic phenotype. Pro-fibrotic transition of MCs—mesothelial-to-mesenchymal transition (MMT), and fibroblasts activation to myofibroblasts are interconnected to changes in cellular metabolism and culminate in the deposition of extracellular matrix (ECM) in the form of fibrotic tissue between injured sides in the abdominal cavity. However, ECM is not only a mechanical scaffold of the newly synthetized tissue but reciprocally affects fibrosis development. Hyaluronan (HA), an important component of ECM, is a non-sulfated glycosaminoglycan consisting of N-acetyl-D-glucosamine (GlcNAc) and D-glucuronic acid (GlcUA) that can affect the majority of processes involved in PA formation. This review considers the role of endogenously produced HA in the context of different fibrosis-related pathologies and its overlap in the development of PA.
Highlights
Peritoneal adhesions (PA) represent one of the major complications following intraabdominal and pelvic surgery leading to symptoms such as abdominal pain, bowel obstruction and infertility
There are studies elucidating the involvement of endogenous HA in different inflammation and fibrosis-related conditions in the peritoneal membrane and abdominal cavity, processes connected to PA formation
HA leads leads reperfusion to exacerbated inflammation and fibrosis accompanied by increased expression of HA, to exacerbated inflammation and fibrosis accompanied by increased expression of HA, CD44, α-Smooth muscle actin and collagen I and III [104]
Summary
Peritoneal adhesions (PA) represent one of the major complications following intraabdominal and pelvic surgery leading to symptoms such as abdominal pain, bowel obstruction and infertility. PA are formed randomly among organs distant from the site of the mechanical disruption. Their formation is currently recognized to be driven by a complex process where a disruption of the mesothelial layer and its underlying structures in the peritoneal membrane and hypoxia, inflammation, and deregulated coagulation/fibrinolysis in the peritoneal cavity participate. Pro-fibrotic transition of mesothelial cells (MCs), forming an inside monolayer of the peritoneal membrane, and a fibroblast-myofibroblast switch of fibroblasts from underlying tissues plays a central role in the alterations of the peritoneal membrane leading to fibrosis [3,4]. This review aims to describe the anticipated effects of endogenously produced HA on fundamental mechanisms responsible for the development of PA inspired by different relevant fibrosis-related pathologies
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