Mast cells (MC) are derived from CD34-positive multipotent bone marrow progenitor cells and they migrate to vascularized tissues where they complete their maturation and acquire a tissue-specific phenotype. Although present in small numbers in the normal kidney, MC accumulate in periglomerular and perivascular areas of the renal cortical tubulointerstitium in progressive nephropathies. The infiltration of MC was correlated with the degree of tubulointerstitial fibrosis and poor disease outcome, regardless of the underlying causes. Consequently, it was readily suggested that MC could contribute to the process of renal deterioration through the participation in tubulointerstitial fibrosis. Accordingly, once activated, MC secrete numerous vasoactive, pro-inflammatory and profibrotic mediators that have already been implicated in organ fibrosis. Therefore, MC targeting may represent a novel therapeutic approach to halt the progression of kidney fibrosis.
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