Fibrosis of the Kidney: Mechanisms of Progression and Its Regulation / Japan Scar Workshop


Papers of The 4th Japan Scar Workshop
9. Fibrosis of the Kidney: Mechanisms of Progression and Its Regulation Takashi Wada Division of Blood Purification, Kanazawa University Hospital, Kanazawa, Japan
Progressive fibrosis is a common pathological finding in various organs, resulting in organ failure. Recently, bone marrow-derived fibrocytes, which express leukocyte markers as well as mesenchymal markers, have been shown to rapidly enter sites of tissue injury and contribute to the pathogenesis of various fibrotic diseases. We have uncovered that fibrocytes migrate into the kidney in response to chemokine system and contribute to kidney fibrosis in mice. In addition, the blockade chemokine system, such as CCL21/CCR7 signaling pathways reduced kidney fibrosis. Furthermore, fibrocytes may be involved in the progression of human kidney diseases, especially in fibrosis. Receptor signaling for angiotensin II, AT1 receptor/AT2 receptor may contribute to the pathogenesis of kidney fibrosis by at least two mechanisms: (1) by regulating the number of fibrocytes in bone marrow, and (2) by activation of fibrocytes. Thus, these findings suggest that fibrocytes contribute to the pathogenesis of kidney fibrosis, indicating that regulating fibrocytes may provide a novel therapeutic benefit for kidney fibrosis.
<< BACK	PAGE TOP