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Fibrosis Research: Methods and Protocols (Methods in Molecular Medicine)

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Fibrosis or scar, defined pathologically as inappropriate repair by connective tissue, is increasingly recognized as an important feature of many chronic diseases (Table 1), and as such, represents an enormous health burden. The United States government estimates that 45% of deaths in the United States can be attributed to fibrosing disorders. Fibrosis can affect virtually every tissue and organ system. Traditionally, fibrosis has been viewed as the irreversible, end-stage sequel to a multitude of diverse disease processes (Table 2). Excessive scarring following physical, thermal, metabolic, ischemic, infectious, inflammatory, or immunological injury can occur in any part of the body, and can cause destruction of the affected structures. Fibrotic tissue is characterized by a loss of normal architecture, paucity of stromal cells, and replacement of blood vessels and other essential parenchymal structures by dense, homogeneous, and increasingly stable extracellular matrix. The scar is composed primarily of type I collagen, but types III and IV collagens, proteoglycans, fibronectin, glycoproteins, and matricellular proteins are also prominent. The process leads to progressive distortion of tissue architecture with consequent dysfunction and ultimate failure of fibrotic organs. Many of the key morphological features of fibrosis are common to scarring affecting the lungs, the liver, the kidneys, the heart, or the skin.

Fibrosis is the “dark side” of normal tissue repair. Following injury, a complex and tightly orchestrated repertoire of cellular responses is called into play, and normally the wound is rapidly and efficiently repaired. This process is spatially and temporally self-limited. In contrast, under some conditions repair is excessive, resulting in pathological scar formation. The pathogenesis of fibrosis remains poorly understood. Fibrosis involves a “fibrogenic cascade” integrating multiple molecular pathways and cellular targets. Historically, the link between inflammation and fibrosis has been emphasized, providing the rationale for anti-inflammatory or immunosuppressive therapies for fibrosis. It has become increasingly evident that these types of interventions are generally ineffective. The lack of effective treatments, and the high mortality and increasing morbidity attributed to chronic fibrotic diseases, has stimulated an explosion of research into the cellular, molecular, and genetic basis of fibrosis.
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