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J Am Soc Nephrol
2013[Jun]; 24
(7
): 1034-9
PMID23641054
show ga
A major hallmark of chronic kidney injury is fibrosis, which is characterized by
increased accumulation of extracellular matrix components that replace the
damaged tissue. Normally, the synthesis and degradation of extracellular matrix
components are finely regulated; however, when matrix replacement goes unchecked,
there is unwanted and irreversible tissue scarring with consequent organ damage,
organ failure, and, in certain cases, death. Many factors, including cell-matrix
interactions, play a role in the development of renal fibrosis. Cell-matrix
interactions are made possible by integrins, a family of transmembrane receptors
that, upon binding to the extracellular matrix, activate intracellular signaling.
Thus, they control various cell functions, including survival, proliferation,
migration, and matrix homeostasis. Genetic mutations in humans and the
development of animal models lacking integrins in selective parts of the kidney
have improved our understanding of molecular mechanisms and pathways controlling
matrix remodeling in kidney disease. Here we outline the major integrins involved
in kidney disease and some of the major molecular mechanisms whereby integrins
contribute to kidney fibrosis.
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