Sepsis-induced disseminated intravascular coagulation (DIC) carries approximately 44% mortality and has no targeted mechanistic therapy. Stable isotope tracer data show whole-blood glutathione (GSH) synthesis falling by approximately 60% in sepsis despite paradoxically elevated cysteine flux, consistent with enzymatic failure at the glutamate-cysteine ligase (GCL) step rather than substrate shortage. We propose that GCL failure may unify endothelial coagulopathy and innate immune dysfunction in...

Sepsis‑induced liver injury (SLI) is a life‑threatening complication of sepsis characterized by microcirculatory dysfunction, oxidative stress, excessive inflammation, and immune dysregulation. However, the role of ErbB2 interacting protein (Erbin) in SLI remains unclear. In the present study, the functional role and underlying mechanism of Erbin were investigated in a cecal ligation and puncture (CLP)‑induced mouse model of SLI using wild‑type and Erbin‑knockout (Erbin‑/‑) mice, together with...

BACKGROUND: Sepsis-induced coagulopathy is characterised by consumptive coagulation abnormalities and resistance to fibrinolysis, which is increasingly recognised as a driver of microvascular thrombosis, organ dysfunction and mortality. The molecular determinants of the fibrinolysis-resistant phenotype remain incompletely defined.

Reduced early mortality in sepsis and severe injuries led to the formation of a cohort of patients with chronic critical conditions (diseases). One of the mechanisms of chronization of acute critical conditions is the development of persistent inflammation, immunosuppression and catabolism syndrome (PICS). Diagnosis of PICS is currently based on clinical and laboratory markers, whereas morphological changes insufficiently studied. Lack of pathogenesis and morphogenesis understanding makes it...