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10.1007/s00441-016-2407-9

http://scihub22266oqcxt.onion/10.1007/s00441-016-2407-9
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C5010580!5010580!27139180
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suck abstract from ncbi

pmid27139180      Cell+Tissue+Res 2016 ; 365 (3): 511-9
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  • ?v integrins: key regulators of tissue fibrosis #MMPMID27139180
  • Conroy KP; Kitto LJ; Henderson NC
  • Cell Tissue Res 2016[]; 365 (3): 511-9 PMID27139180show ga
  • Chronic tissue injury with fibrosis results in the disruption of tissue architecture, organ dysfunction and eventual organ failure. Therefore, the development of effective anti-fibrotic therapies is urgently required. During fibrogenesis, complex interplay occurs between cellular and extracellular matrix components of the wound healing response. Integrins, a family of transmembrane cell adhesion molecules, play a key role in mediating intercellular and cell-matrix interactions. Thus, integrins provide a major node of communication between the extracellular matrix, inflammatory cells, fibroblasts and parenchymal cells and, as such, are intimately involved in the initiation, maintenance and resolution of tissue fibrosis. Modulation of members of the ?v integrin family has exhibited profound effects on fibrosis in multiple organs and disease states. In this review, we discuss the current knowledge of the mechanisms of ?v-integrin-mediated regulation of fibrogenesis and show that the therapeutic targeting of specific ?v integrins represents a promising avenue to treat patients with a broad range of fibrotic diseases.
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