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Acknowledgements We are sincerely thankful to Prof

Together, this may indicate that chronic oxidative stress caused by the loss of Fh1 exerts its pathophysiological consequence of renal cyst formation in these mice through oxidation of proteins involved in metabolic processes and in maintaining tissue architecture, such as the cytoskeletal and extracellular matrix proteins, despite ROS-scavenging by intracellular, vascular, and urinary proteins