Abstract
Significance: Fibrosis is the endpoint of chronic disease in multiple organs, including the skin, heart, lungs, intestine, liver, and kidneys. Pathologic accumulation of fibrotic tissue results in a loss of structural integrity and function, with resultant increases in morbidity and mortality. Understanding the pathways governing fibrosis and identifying therapeutic targets within those pathways is necessary to develop novel antifibrotic therapies for fibrotic disease.Recent Advances: Given the connection between inflammation and fibrogenesis, Interleukin-10 (IL-10) has been a focus of potential antifibrotic therapies because of its well-known role as an anti-inflammatory mediator. Despite the apparent dissimilarity of diseases associated with fibrotic progression, pathways involving IL-10 appear to be a conserved molecular theme. More recently, many groups have worked to develop novel delivery tools for recombinant IL-10, such as hydrogels, and cell-based therapies, such as ex vivo activated macrophages, to directly or indirectly modulate IL-10 signaling.Critical Issues: Some efforts in this area, however, have been stymied by IL-10's pleiotropic and sometimes conflicting effects. A deeper, contextual understanding of IL-10 signaling and its interaction with effector cells, particularly immune cells, will be critical to future studies in the field.Future Directions: IL-10 is clearly a gatekeeper of fibrotic/antifibrotic signaling. The development of novel therapeutics and cell-based therapies that capitalize on targets within the IL-10 signaling pathway could have far-reaching implications for patients suffering from the consequences of organ fibrosis.
Highlights
AND OVERVIEW Cellular injury and fibrogenesisDespite the diverse means by which the body sustains injury, most organs repair themselves through a common pathway that leads to the formation of collagen deposition or fibrogenesis (Fig. 1)
sometimes opposing effects depending on organ system
sometimes contradictory effects of IL-10 in this process should not come as a surprise
Summary
Understanding the pathways governing fibrosis and identifying therapeutic targets within those pathways is necessary to develop novel antifibrotic therapies for fibrotic disease. The development of novel therapeutics and cell-based therapies that capitalize on targets within the IL-10 signaling pathway could have far-reaching implications for patients suffering from the consequences of organ fibrosis. TRANSLATIONAL RELEVANCE prior work on IL-10 in fibrosis comes from many fields in studying many different disease processes, there appear to be unifying themes within the literature. This review seeks to consolidate the literature on IL-10 signaling and multiorgan fibrosis with the intention of identifying common pathways between various pathologies, which may lead to novel therapeutic targets. New research on the cellular context of IL-10 signaling has led to novel cell-based therapies that have the potential to revolutionize the treatment of fibrosis in multiple organs
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