Long Non-coding RNA Neat1, NLRP3 Inflammasome, and Acute Kidney Injury.
Rui XueWai Han YiuKam Wa ChanSarah W Y LokYixin ZouJingyuan MaHong-Yu LiLoretta Y Y ChanXiao Ru HuangKar Neng LaiHui Yao LanSydney Chi-Wai TangPublished in: Journal of the American Society of Nephrology : JASN (2024)
Our findings demonstrate a pathogenic role of Neat1 induction in human and mice during AKI with alleviation of kidney injury in 3 experimental models of septic and aseptic AKI after knockdown of Neat1. LPS/TLR4-induced Neat1 overexpression in tubular epithelial cells increases the inflammatory response by binding with the scaffold protein, Rack1, to activate NLRP3 inflammasomes.
Keyphrases
- acute kidney injury
- inflammatory response
- long non coding rna
- nlrp inflammasome
- cardiac surgery
- poor prognosis
- high glucose
- endothelial cells
- toll like receptor
- lipopolysaccharide induced
- lps induced
- cell proliferation
- immune response
- binding protein
- type diabetes
- drug induced
- induced pluripotent stem cells
- metabolic syndrome
- high fat diet induced
- protein protein
- small molecule