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The role of cell plasticity in progression and reversal of renal fibrosis
Author(s) -
Dussaule JeanClaude,
Guerrot Dominique,
Huby AnneCécile,
Chadjichristos Christos,
Shweke Nasim,
Boffa JeanJacques,
Chatziantoniou Christos
Publication year - 2011
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2011.00760.x
Subject(s) - myofibroblast , fibrosis , extracellular matrix , kidney disease , angiotensin ii , vascular smooth muscle , pathology , medicine , kidney , mesenchymal stem cell , disease , cancer research , biology , endocrinology , microbiology and biotechnology , smooth muscle , receptor
Summary The need for novel insights into the mechanisms of progression of renal disease has become urgent during the last several years because of the increasing incidence of chronic renal disease worldwide. Independent of the underlying disease, the subsequent progression of renal fibrosis is characterized mainly by both an exaggerated synthesis and abnormal accumulation of extracellular matrix proteins produced by mesenchymal cells within the kidney. These cells are mainly myofibroblasts deriving from a variety of renal cells such as vascular smooth muscle, mesangial, resident stem, tubular epithelial, vascular endothelial cells or pericytes. The appearance of myofibroblasts is a reversible process, as suggested by studies in experimental models showing regression of renal fibrosis during therapy with antagonists and/or blockers of the renin–angiotensin system. An additional factor that can also affect the mechanisms of progression/regression of fibrosis is the plasticity of podocytes controlling glomerular filtration.