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Here we show that necroptosis plays a role in a second wave of tubular cell death in experimental toxic AKI. This second wave of death is triggered by TWEAK activation of the Fn14 receptor and contributes to persistence of injury. We previously observed that the initial wave of cell death was ferroptosis dependent and necroptosis independent. The identification of a pathway contributing to AKI persistence may facilitate the design of therapies, as exemplified by the protection afforded by RIPK1 inhibitors when administered after AKI had been induced.<\/jats:p>","DOI":"10.1073\/pnas.1716578115","type":"journal-article","created":{"date-parts":[[2018,3,27]],"date-time":"2018-03-27T11:20:57Z","timestamp":1522149657000},"page":"4182-4187","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":147,"title":["TWEAK and RIPK1 mediate a second wave of cell death during AKI"],"prefix":"10.1073","volume":"115","author":[{"given":"Diego","family":"Martin-Sanchez","sequence":"first","affiliation":[{"name":"Red de Investigacion Renal (REDINREN), Research Institute\u2013Fundaci\u00f3n Jim\u00e9nez D\u00edaz, Autonomous University of Madrid (UAM), 28040 Madrid, 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