Hypertension and nephrology

[Signaling pathways in renal fibrosis]


SEPTEMBER 20, 2014

Hypertension and nephrology - 2014;18(03-04)

[Myofibroblasts are the main effector cells of tissue fibrosis in chronic kidney disease. These cells are the main source of collagen rich extracellular matrix in the fibrous tissue. Recent hypotheses suggest that pericytes are the major progenitors of myofibroblasts. Platelet derived growth factor, transforming growth factor β and Wingless/Int signaling pathways play important role in pericyte activation. There are experimental evidences that blocking this pathways inhibits tissue fibrosis, therefore they might be targets for the development of antifibrotic drugs in the future.]



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Hypertension and nephrology



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Related contents

Hypertension and nephrology

[The importance of epithelial-mesenchymal transition in kidney fibrosis]


[Epithelial-mesenchymal transition (EMT) plays a central role in physiological and pathological processes of embryogenesis, carcinogenesis and tissue fibrosis. During EMT epithelial cells may transform to myofibroblasts, which are the effector cells of fibrosis. In our summary the process of EMT and its medical importance will be reviewed in relation to renal fibrosis. Regardless of the initiating cause the final common mechanism of organ fibrosis is similar in the different chronic renal diseases. It always involves major inflammatory responses, however the molecular mechanisms involved are still elusive. The EMT now takes centre stage as the point of convergence between inflammation and the progression of degenerative fibrotic diseases. Understanding the pathomechanism of EMT and the significance of signalling pathways involved in this process may lead to a new therapeutic approach in the treatment of chronic renal diseases.]

Hypertension and nephrology

[Molecular mechanisms leading to renal fibrosis: the origin of myofibroblasts]

HIMER Leonóra, SZIKSZ Erna, KOVÁCS S. Krisztián, ÓNODY Anna, Reusz Anna, REUSZ György, FEKETE Andrea, TULASSAY Tivadar, VANNAY Ádám

[There are about a quarter of million patients who need chronic renal replacement therapy in Europe, and the estimated number of patients with chronic kidney disease is about tenfold higher. Interestingly, regardless of the initiating cause the mechanism of fibrosis is similar to each other in the different chronic kidney diseases. In general, the damaged glomerular or tubular cells release danger signals and produce chemotactic stimuli, which trigger the rapid recruitment of leukocytes. The infiltrating immune cells and the damaged renal cells then produce high levels of proinflammatory cytokines, growth factors, chemokines and adhesion molecules which contribute to glomerular/tubular injury, accumulation of further leukocytes and myofibroblasts, which are the effector cells of renal fibrosis. However the origin of myofibroblasts is still controversial. Recent hypotheses suggest that they are originated from different renal cells, such as epithelial and endothelial cells, pericytes or bone marrow derived fibrocytes. The myofibroblasts thus generated serve as key cellular mediators of renal fibrosis. Myofibroblasts have migratory capacity, are resistant to apoptosis, produce several growth factors and cytokines and according to our present knowledge these cells are the main source of collagen-I and -III rich extracellular matrix in the fibrous tissue. Organ fibrosis is characterized with excessive deposition of extracellular matrix leading to glomerular sclerosis and renal tubulointerstitial fibrosis. The excessive deposition of fibrous tissue replaces healthy kidney tissue; nephrons disappear and kidney function declines gradually. In this article the knowledge is summarized on the molecular changes leading to the generation of renal myofibroblasts.]

Hypertension and nephrology

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