Nov 19, 2019

D-Ribose Induces Podocyte NLRP3 Inflammasome Activation and Glomerular Injury via AGEs/RAGE Pathway

Frontiers in Cell and Developmental Biology
Jinni HongPin-Lan Li


D-ribose levels are demonstrated to be increased in type II diabetes mellitus and increased blood D-ribose is involved in the development of diabetic complications such as diabetic encephalopathy and nephropathy. However, the mechanism mediating the pathogenic role of D-ribose in nephropathy remains poorly understood. Given that D-ribose was reported to induce advanced glycation end products (AGEs) formation, the present study tested whether D-ribose induces NLRP3 activation and associated glomerular injury via AGEs/receptor of AGEs (RAGE) signaling pathway. In vivo, C57BL/6J and Asc-/- mice were treated with D-ribose with or without AGEs inhibitor. Administration of D-ribose daily for 30 days was found to induce NLRP3 inflammasome formation in glomerular podocyte, as shown by increased co-localization of NLRP3 with apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) or caspase-1. This D-ribose-induced NLRP3 inflammasome formation was accompanied by its activation as evidenced by increased IL-1β production, a major product of NLRP3 inflammasome. Corresponding to NLRP3 inflammasome activation, D-ribose led to significant glomerular injury in mice. All these D-ribose-induced glomerular inflammaso...Continue Reading

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Mentioned in this Paper

Diabetes Mellitus, Non-Insulin-Dependent
In Vivo
Gene Deletion
Administration Procedure
CIAS1 protein, mouse
NLRP3 gene

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis