circGAB1 Activates Autophagy to Promote Sepsis-Associated Acute Kidney Injury by Interacting with ELAVL1 to Activate the HMGB3/β-catenin Signaling Pathway.
Jul 2026· Applied Biochemistry and Biotechnology· 0 citations· 31 references
Medicine
TL;DR
Analysis of the public GEO dataset revealed that circGAB1 was significantly upregulated in SA-AKI samples, and its high expression was also verified in SA-AKI model cells, and it exhibited a nucleocytoplasmic subcellular localization pattern.
It is suggested that METTL3/FOSL1-associated regulatory responses may participate in S-AKI through m6A-related regulation, contributing to inflammatory and autophagy-related alterations.
Feifei Shao, Junhao Pan, Qing-qing Yan et al.· Archives of Biochemistry and...· 0 citations
A maladaptive NF-κB/miR-378c/IRG1 axis in septic AKI is defined, where inflammation-induced miR-378c silences a key metabolic protector in tubular cells and represents a promising therapeutic strategy to preserve renal function during sepsis.
Lulu Zhou, Xiang Zhou, Hong-Mei Deng et al.· Renal Replacement Therapy· 0 citations
It is reported that Mir452 protects kidney tubular cells in septic AKI by repressing APAF1 and associated caspase activation and thereby inhibiting apoptosome-mediated CASP9 activation to preserve macroautophagy/autophagy.
Assessment of circTMCC1 expression in human coronary artery segments, peripheral blood mononuclear cells from CAD patients, M1 macrophages, and an AMI mouse model suggests it may serve as a promising diagnostic biomarker and therapeutic target for CAD and AMI, potentially improving prognosis.
Mengmeng Ren, Shu He, Mengyang Duan et al.· Cell Death Discovery· 0 citations
This article examined the effect of DLX6-AS1 on ischemia perfusion-induced myocardial injury caused by necroptosis and the underlying potential mechanism and identified the possible mechanism by overexpressing and inhibiting DLX6-AS1 expression.
Yan-Ping Su, Li-Ting Mu, Lei Wang et al.· Scientific Reports· 0 citations
Salidroside exerts protective effects in sepsis-associated ALI, which may be associated with modulation of the ERK/FoxO3a signaling axis, improvement of impaired autophagic flux, and maintenance of mitochondrial function.