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Tonnus, W.* ; Maremonti, F.* ; Belavgeni, A.* ; Latk, M.* ; Brucker, A.J.* ; von Maessenhausen, A.* ; Meyer, C.* ; Locke, S.* ; Gembardt, F.* ; Beer, K.* ; Hoppenz, P.* ; Hugo, C.* ; Anders, H.J.* ; Bornstein, S.R. ; Shao, F.W.* ; Linkermann, A.*

Gasdermin D-deficient mice are hypersensitive to acute kidney injury.

Cell Death Dis. 13:792 (2022)

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Signaling pathways of regulated necrosis, such as necroptosis and ferroptosis, contribute to acute kidney injury (AKI), but the role of pyroptosis is unclear. Pyroptosis is mediated by the pore-forming protein gasdermin D (GSDMD). Here, we report a specific pattern of GSDMD-protein expression in the peritubular compartment of mice that underwent bilateral ischemia and reperfusion injury (IRI). Along similar lines, the GSDMD-protein expression in whole kidney lysates increased during the first 84 h following cisplatin-induced AKI. Importantly, unlike whole kidney lysates, no GSDMD-protein expression was detectable in isolated kidney tubules. In IRI and cisplatin-induced AKI, GSDMD-deficient mice exhibited hypersensitivity to injury as assessed by tubular damage, elevated markers of serum urea, and serum creatinine. This hypersensitivity was reversed by a combined deficiency of GSDMD and the necroptosis mediator mixed lineage kinase domain-like (MLKL). In conclusion, we demonstrate a non-cell autonomous role for GSDMD in protecting the tubular compartment from necroptosis-mediated damage in IRI.

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