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Fig. 3 | Inflammation and Regeneration

Fig. 3

From: Resident fibroblasts in the kidney: a major driver of fibrosis and inflammation

Fig. 3

Fibroblasts have two jobs during CKD: fibrosis and inflammation. Resident fibroblasts critically contribute to fibrosis and the persistence of inflammation in the injured kidney [3]. Upon injury, resident fibroblasts transdifferentiate into myofibroblasts, which produce a large amount of ECM protein and pro-inflammatory cytokines/chemokines, at the cost of EPO production. Moreover, in the aging milieu, resident fibroblasts also transdifferentiate into several distinct phenotypic fibroblasts, which orchestrate TLT formation. In response to injury, resident fibroblasts differentiate into RALDH-positive fibroblasts, which induce transdifferentiation of other fibroblasts into p75NTR-positive fibroblasts with three phenotypes, which include CXCL13- and CCL19-producing fibroblasts. In the later phase of TLT formation, some of these p75NTR-positive fibroblasts lose this expression and mature into CD21/CXCL13-positive FDCs

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