Fibrosis, a common pathway to organ failure: angiotensin II and tissue repair.

摘要: Abstract For heart, kidneys, lungs and liver alike, fibrosis represents a common pathway to their failure. Understanding pathophysiologic mechanisms involved in organ are therefore of considerable interest, particularly given the potential for protective pharmacological strategies. Tissue repair involves inflammatory cells, including members monocyte/macrophage lineage, integral initiating process; myofibroblasts, phenotypically transformed interstitial fibroblasts, responsible collagen turnover fibrous tissue formation. Each these cellular events microenvironment associated with molecular that lead de novo generation angiotensin II (ANG II). In an autocrine/paracrine manner, this peptide regulates expression TGF-beta 1 via (AT1) receptor-ligand binding. It is cytokine contributes phenotypic conversion fibroblasts myofibroblasts (myoFb) myofibroblast collagen. Angiotensin-converting enzyme (ACE) inhibition or AT1 receptor antagonism each prevent many responses eventuate have been found be interventions.