Fibroblasts: Key Mediators of Regeneration, Inflammation and Fibrosis (Volume II)

Dear Colleagues,

Fibroblasts are spindle-shaped, site-specific cells of mesenchymal origin in the interstitial spaces of organs and part of the connective tissue. They include synovial fibroblasts, dermal fibroblasts, and bone marrow stromal cells. Fibroblasts are the primary source of interstitial extracellular matrix (ECM) proteins, mainly including collagen fibers, which, together with the proteoglycans that are also formed, provide increased strength for the extracellular matrix, forming a scaffold for cells. In addition to providing a scaffold for cells, ECM proteins play key roles in determining cell phenotype and function. Alongside ECM proteins, fibroblasts secrete proteolytic enzymes, growth factors, cytokines, and chemokines. Finally, fibroblasts adhere to and contract connective tissue and are capable of transdifferentiating into activated proliferative fibroblasts or myofibroblasts. Thus, it is not surprising that they are key players in acute and chronic inflammatory processes such as wound healing and fibrosis, cirrhosis dermatitis, and arthritis. In physiological ECM maintenance, the fibroblast repair program is self-limiting. By contrast, pathological fibrosis is characterized by uncontrolled fibroblast activation that results in exaggerated and persistent ECM accumulation and remodeling. The responses of fibroblasts to activation include proliferation, fibrinogenesis, and the release of cytokine and proteolytic enzymes. Fibroblasts are critical components of the granulation tissue of healing wounds or broken bones during soft callus formation. In the healing wound, the number of fibroblasts increases, while the number of inflammatory cells decreases. Increased numbers of fibroblasts or myofibroblasts occur primarily due to the local proliferation of local fibroblasts or other cells of mesenchymal origin such as pericytes, liver perisinusoidal cells, kidney mesangial cells, and epithelial cells after epithelial–mesenchymal transition. Myofibroblasts can also develop from circulating precursors such as mononuclear cells and circulating fibrocytes. Peripheral blood fibrocytes rapidly enter the site of injury at the same time as circulating inflammatory cells. Although they are important players in the process of wound healing, fibroblasts are involved in regulating many chronic inflammatory diseases such as rheumatoid arthritis, primary biliary cirrhosis, atherosclerosis, kidney interstitial fibrosis, and peritoneal fibrosis. This Special Issue will focus on fibroblasts and their critical role in a variety of diseases. In particular, for this Special Issue, contributions dealing with the characterization of fibroblasts, their mechanistic and metabolic switches from tissue-resident fibroblasts to proliferative myofibroblasts, fibrometabolism, the homing of fibrocytes to sites of inflammation, model systems of fibrosis, and therapeutic interference to prevent or treat fibrosis are highly encouraged.

Dr. Timo Gaber
Guest Editor

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