Renal epithelial cells show remarkable regenerative capacity to recover from acute injury, which involves specific phenotypic changes, but also significant profibrotic tubule-interstitial crosstalk. Tubule-derived profibrotic stimuli and subsequent myofibroblast activation and extracellular matrix deposition have been linked closely with decline of renal function and nephron loss. However, recent data have questioned the view of purely detrimental effects of myofibroblast activation in the injured kidney and even suggested its beneficial role for epithelial regeneration. This article reviews the current understanding of the underlying mechanisms of tubular cell turnover, new suggested pathways of proregenerative tubular-interstitial crosstalk, and relevant insights of proliferation-enhancing effects of myofibroblasts on epithelial cells in nonrenal tissues.
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http://dx.doi.org/10.1016/j.semnephrol.2020.01.012 | DOI Listing |
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