inhibition restored the EPO-producing capability and fibroblastic signatures (including CD73 expression, Figure) to the primary myofibroblasts obtained from the urine of a patient with CKD.Conclusion: HDAC inhibition promotes the dedifferentiation of renal myofibroblasts into fibroblasts and induces apoptosis in activated, highly ECM-producing myofibroblasts.This strategy offers a novel therapeutic approach that could potentially not only suppress renal fibrosis but also ameliorate associated tubular damage and EPO deficiency.
Wang et al. (Wed,) studied this question.