CONCLUSION: Among patients with T2D who developed sepsis, prior GLP-1RA use was associated with lower mortality and select cardiovascular/renal risks than prior SGLT2i use, though roughly half of secondary outcomes showed no significant difference. Exposure was defined at the drug-class rather than individual-agent level, and modest E-values alongside baseline imbalances before matching suggest residual confounding cannot be excluded. These hypothesis-generating findings warrant confirmation in...

INTRODUCTION: Septic shock, a severe, life-threatening infection resulting in organ failure, has seen no successful, novel therapies emerge in the past two decades. In addition to hypoperfusion and inflammation, organ dysfunction in septic shock is caused by microvascular, mitochondrial, and immune dysfunction. Animal studies support the use of hyperbaric oxygen treatment to improve mitochondrial function and reduce the inflammatory cascade, suggesting a potential role for hyperbaric oxygen in...

Sepsis is a deadly syndrome arising from overactivation of the immune system in response to a pathogen. Severe sepsis can result in sepsis-associated encephalopathy (SAE) that significantly contributes to morbidity and long-term cognitive impairment. Studying the molecular underpinnings of SAE in the human brain is challenging, and rodent models have limited translational applicability due to significant neuroanatomical and immune differences. To bridge this gap, we employed a Yorkshire pig...

CONCLUSIONS: Preclinical research on sepsis-induced capillary leak is characterized by methodological heterogeneity, a disproportionately high rate of studies reporting capillary leak reduction, and an overreliance on endotoxemia models. Bridging the translational gap will require standardized assessment of capillary leak, broader use of live-pathogen large-animal models, post-treatment dosing paradigms, and clinical trials enriched for endothelial dysfunction.