LIGHT aggravates sepsis‐associated acute kidney injury via TLR4‐MyD88‐NF‐κB pathway

• Published in: Journal of cellular and molecular medicine Vol. 24; no. 20; pp. 11936 - 11948
• Main Authors: Zhong, Yu, Wu, Shun, Yang, Yan, Li, Gui‐qing, Meng, Li, Zheng, Quan‐you, Li, You, Xu, Gui‐lian, Zhang, Ke‐qin, Peng, Kan‐fu
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.10.2020; John Wiley and Sons Inc
• Subjects: acute kidney injury; Acute Kidney Injury - metabolism; Acute Kidney Injury - pathology; Animals; Apoptosis; Cell injury; Cell Line; Down-Regulation; Fc receptors; Gene expression; Humans; Immunoregulation; Inflammation; Inflammation - pathology; Inflammation Mediators - metabolism; Kidneys; Laboratory animals; LIGHT; Lipopolysaccharides; Metastases; Mice, Knockout; Models, Biological; Morbidity; MyD88 protein; Myeloid Differentiation Factor 88 - metabolism; NF-kappa B - metabolism; NF‐κB; Original; Pathophysiology; Proteins; Reagents; Renal function; Sepsis; Sepsis - metabolism; Signal Transduction; Survival Analysis; TLR4; TLR4 protein; Toll-Like Receptor 4 - metabolism; Toll-like receptors; Tumor necrosis factor; Tumor Necrosis Factor Ligand Superfamily Member 14 - deficiency; Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism; Tumors; Beijing China; United States > US; China; Japan; NF-κB; acute kidney injury; TLR4; sepsis; LIGHT

Sepsis‐associated acute kidney injury (SA‐AKI) is a common clinical critical care syndrome. It has received increasing attention due to its high morbidity and mortality; however, its pathophysiological mechanisms remain elusive. LIGHT, the 14th member of the tumour necrosis factor (TNF) superfamily...