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In eNOS / mice, RIPK3 blockade or RIPK3 deficiency has been shown to reduce kidney inflammatory cell infiltration and reduce myofibroblast activation and collagen deposition (88)

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As the essential eNOS cofactor tetrahydrobiopterin (BH 4 ) is susceptible for oxidation, a landmark study by David Harrison's group 62 was able to proof the concept that superoxide produced by the Nox may indeed trigger eNOS uncoupling in the experimental animal model of DOCA-salt hypertension