Immune microenvironment changes of liver cirrhosis: emerging role of mesenchymal stromal cells

Abstract

Cirrhosis is a progressive and diffuse liver disease characterized by liver tissue fibrosis and impaired liver function. This condition is brought about by several factors, including chronic hepatitis, hepatic steatosis, alcohol abuse, and other immunological injuries. The pathogenesis of liver cirrhosis is a complex process that involves the interaction of various immune cells and cytokines, which work together to create the hepatic homeostasis imbalance in the liver. Some studies have indicated that alterations in the immune microenvironment of liver cirrhosis are closely linked to the development and prognosis of the disease. The noteworthy function of mesenchymal stem cells and their paracrine secretion lies in their ability to promote the production of cytokines, which in turn enhance the self-repairing capabilities of tissues. The objective of this review is to provide a summary of the alterations in liver homeostasis and to discuss intercellular communication within the organ. Recent research on MSCs is yielding a blueprint for cell typing and biomarker immunoregulation. Hopefully, as MSCs researches continue to progress, novel therapeutic approaches will emerge to address cirrhosis.

Mesenchymal Stem Cells Alleviate Mouse Sepsis-Induced Cardiomyopathy by Inhibiting the NR1D2/LCN2 Pathway

“…Through the paracrine secretion of various cytokines, MSCs can suppress proinflammatory reactions and enhance anti-inflammatory effects, thereby contributing to the treatment of inflammatory and immune-related disorders. 6,7 In the context of sepsis, MSCs exhibit anti-inflammatory properties, immune regulatory functions, apoptosis inhibition, antibacterial activity, and promotion of angiogenesis, making them a valuable subject of investigation in clinical research. 8 In the rat sepsis model, MSCs-derived exosomes can inhibit cardiomyocyte apoptosis, improve rat myocardial function, and inhibit inflammatory response.…”