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Abstract Endothelial dysfunction contributes to multi-organ injury in sepsis, but the underlying mechanisms remain incompletely understood. Here we show that endothelial ubiquitin-specific protease 28 (USP28) is increased in patients with sepsis and in male mice in a murine polymicrobial sepsis model. Mechanistically, USP28 stabilizes non-muscle myosin heavy chain IIA (NMMHC IIA) by removing K48-linked ubiquitination at K1413.
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