Open AccessInhibition of Hyperhomocysteinemia-Induced Inflammasome Activation and Glomerular Sclerosis by NLRP3 Gene Deletion
Author(s) -
Min Xia,
Sabena M. Conley,
Guangbi Li,
PinLan Li,
Krishna M. Boini
Publication year - 2014
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000363046
Subject(s) - podocin , inflammasome , podocyte , nephrin , hyperhomocysteinemia , endocrinology , knockout mouse , medicine , small hairpin rna , chemistry , transfection , microbiology and biotechnology , receptor , apoptosis , kidney , homocysteine , biology , proteinuria , gene knockdown , biochemistry , gene
Hyperhomocysteinemia (hHcys) has been reported to initiate Nod-like receptor protein 3 (NLRP3) inflammasome formation and activation in podocytes, leading to glomerular dysfunction and sclerosis. However, it remains unknown whether Nlrp3 gene is critical for the formation and activation of inflammasomes in glomeruli of hHcys mice.