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2011 ; 7
(12
): 684-96
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Cellular and molecular mechanisms of renal fibrosis
#MMPMID22009250
Liu Y
Nat Rev Nephrol
2011[Oct]; 7
(12
): 684-96
PMID22009250
show ga
Renal fibrosis, particularly tubulointerstitial fibrosis, is the common final
outcome of almost all progressive chronic kidney diseases. Renal fibrosis is also
a reliable predictor of prognosis and a major determinant of renal insufficiency.
Irrespective of the initial causes, renal fibrogenesis is a dynamic and
converging process that consists of four overlapping phases: priming, activation,
execution and progression. Nonresolving inflammation after a sustained injury
sets up the fibrogenic stage (priming) and triggers the activation and expansion
of matrix-producing cells from multiple sources through diverse mechanisms,
including activation of interstitial fibroblasts and pericytes, phenotypic
conversion of tubular epithelial and endothelial cells and recruitment of
circulating fibrocytes. Upon activation, matrix-producing cells assemble a
multicomponent, integrin-associated protein complex that integrates input from
various fibrogenic signals and orchestrates the production of matrix components
and their extracellular assembly. Multiple cellular and molecular events, such as
tubular atrophy, microvascular rarefaction and tissue hypoxia, promote scar
formation and ensure a vicious progression to end-stage kidney failure. This
Review outlines our current understanding of the cellular and molecular
mechanisms of renal fibrosis, which could offer novel insights into the
development of new therapeutic strategies.
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