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In a mouse model of endotoxemia, LPS rapidly induced S100A8/A9 release and acute cardiac depression, while genetic deficiency of S100A9 or pharmacological blockade of S100A8/A9 with ABR-238901 prevented or reversed myocardial dysfunction and reduced systemic inflammation (Jakobsson et al., 2023)

Mitochondrial translocation of oxidized cofilin induces caspase-independent necrotic-like programmed cell death of T cells

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