Abstract
Importance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney diseases, inflammatory bowel disease, and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem. According to some estimates about 45% of all deaths are attributed to FDs in the developed world. Independently of their etiology the common hallmark of FDs is chronic inflammation. Infiltrating immune cells, endothelial, epithelial, and other resident cells of the injured organ release an orchestra of inflammatory mediators, which stimulate the proliferation and excessive extracellular matrix (ECM) production of myofibroblasts, the effector cells of organ fibrosis. Abnormal amount of ECM disturbs the original organ architecture leading to the decline of function. Although our knowledge is rapidly expanding, we still have neither a diagnostic tool to detect nor a drug to specifically target fibrosis. Therefore, there is an urgent need for the more comprehensive understanding of the pathomechanism of fibrosis and development of novel diagnostic and therapeutic strategies. In the present review we provide an overview of the common key mediators of organ fibrosis highlighting the role of interleukin-10 (IL-10) cytokine family members (IL-10, IL-19, IL-20, IL-22, IL-24, and IL-26), which recently came into focus as tissue remodeling-related inflammatory cytokines.
Highlights
The significance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney disease (CKD), inflammatory bowel diseases (IBD), and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem [1]
In the case of chronic FDs the sensitive balance between the synthesis and degradation of extracellular matrix (ECM) components is disturbed, and the continuously activated MFs produce an excessive amount of ECM resulting in the replacement of parenchymal tissue by connective tissues
These cytokines can be classified into three subfamilies with different biological functions: (1) IL-10 subfamily represented by IL-10 itself; (2) IL-20 subfamily (IL-19, IL-20, IL-22, IL24, and IL-26) which play a role in host defense mechanisms against bacteria; (3) type III interferons (IFNs): IL-28A, IL28B, and IL-29, which induce antiviral responses
Summary
The significance of chronic fibroproliferative diseases (FDs) including pulmonary fibrosis, chronic kidney disease (CKD), inflammatory bowel diseases (IBD), and cardiovascular or liver fibrosis is rapidly increasing and they have become a major public health problem [1]. In the case of chronic FDs the sensitive balance between the synthesis and degradation of extracellular matrix (ECM) components is disturbed, and the continuously activated MFs produce an excessive amount of ECM resulting in the replacement of parenchymal tissue by connective tissues. This chronic pathogenic remodeling process leads to the destruction of normal organ architecture and consequent decline of its function [5, 6]. Fibrosis with special focus on tissue remodeling-related inflammatory mediators, highlighting the potential pathomechanical role of the members of interleukin-10 (IL-10) cytokine family
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