Results 161 to 170 of about 31,126 (279)

Role of RIPK1/RIPK3/MLKL signalling pathway in sepsis‐associated acute kidney injury

open access: yesExperimental Physiology, EarlyView.
Abstract Sepsis‐associated acute kidney injury (SA‐AKI) is a common clinical syndrome in critically ill patients, and its high mortality rate is closely related to complex pathological mechanisms. Existing studies have shown that the pathophysiological process of SA‐AKI involves complex multi‐mechanism interactions, including an uncontrolled systemic ...
Huijun Yin, Jingyi Wang, Huirong Han
wiley   +1 more source

Effects of tempol on renal medullary tissue hypoxia in an ovine model of Gram‐negative septic acute kidney injury

open access: yesExperimental Physiology, EarlyView.
Abstract Renal arterial infusion of tempol (RAT) at the onset of Gram‐negative sepsis can prevent sepsis‐induced medullary tissue hypoxia and acute kidney injury (AKI). However, it is not known whether treatment with tempol at a clinically relevant time point of sepsis is similarly effective. Thus, we examined whether tempol can reverse renal medullary
Rachel Peiris   +10 more
wiley   +1 more source

Cardamonin Commands the Colonic Metabolite Columbianetin Acetate to Compete Against LPS in Binding HMGB1 in the Kidney, Preventing Lipopolysaccharide‐Induced Renal Tubular Pyroptosis

open access: yesFood Frontiers, Volume 7, Issue 2, March 2026.
Cardamonin upregulate sd the intestinal metabolite columbianetin acetate, which competitively bound HMGB1 to prevent LPS‐induced renal tubular cell pyroptosis (the figure is created with BioRender). ABSTRACT Sepsis‐associated acute kidney injury (SA‐AKI) results in high mortality due to the lack of effective interventions. The current study reports the
Zihui Zhou   +6 more
wiley   +1 more source

Mitochondrial Dysfunction in Propionic Acidemia: A Case‐Report and Review of the Literature

open access: yesJIMD Reports, Volume 67, Issue 2, March 2026.
ABSTRACT Propionic acidemia is an inborn error of metabolism involving an enzymatic defect of propionyl‐CoA carboxylase that results in the build‐up of toxic metabolites which can induce metabolic decompensation. Secondary mitochondrial dysfunction in propionic acidemia has been commonly recognized; however, its clinical presentation and management are
Brandon K. Walther   +5 more
wiley   +1 more source

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