An estimated 10% of the world population has some form of kidney disease. Kidney fibrosis is the final common pathway of progressive kidney diseases, resulting in subsequent massive destruction of normal kidney structure and diminishing the function. The kidney fibrosis is caused by prolonged injury and dysregulation of normal wound healing process associated with an excessive abnormal extracellular matrix deposition. Kidney fibroblasts play a vital role, but the origin of fibroblasts remains to be under intensive discussion. Inflammatory cells and cytokines likely play an important role in fibroblast activation. Furthermore not only the fibroblast, but also any type of kidney cells can become extracellular matrix producing mesenchymal phonotypic cells. Apart from the different cells contributing in the fibrosis, there are many pathways, involved in the initiation and progression of kidney fibrosis. Currently approved therapies are neither pathway nor cell specific in nature, due to which these therapies became ineffective in reducing the fibrosis and are associated with side effects. The understanding of the pathways and cells which are involved in the fibrosis will guide the future therapies to combat the kidney fibrosis.

We invite investigators to contribute original research articles as well as review articles which will stimulate the continuing efforts to understand the molecular pathology underlying kidney fibrosis, the development of newer strategies to treat kidney fibrosis, tissue regeneration, and the evaluation of outcomes. We are particularly interested in articles describing the newer concepts in fibroblast activation process and inflammation and newer strategies in the area of kidney fibrosis and its therapy. Any kinds of disease models are welcome. Potential topics include, but are not limited to:

• Clinical biomarkers
• Advances in genetics/epigenetics
• Newer concepts which can explain fibroblast activation process
• Role of inflammation
• Obstruction/stone leading to fibrosis
• Role of cytokine/chemokines
• Transplant kidney fibrosis
• Diabetic kidney disease
• Hypoxia in kidney fibrosis

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