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Multi-omics integration revealed a high-inflammation, high-oxidation, low-metabolism triad, which is mainly regulated by the Stat1-(2-carboxypropyl)-Cysteamine-C3 interaction axis
The proinflammatory DAMPs molecules released by necroptosis in renal allografts triggered the inflammatory injury, thereby accelerating allograft rejection
Far beyond the 28-day post-reconstitution window
Thoughtful individualization based on patient characteristics, systematic titration allowing tolerance development, and systematic monitoring enables development of personalized protocols delivering optimal outcomes within each individual's physiologic capacity and treatment goals
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