Inflammasome activation and metabolic remodelling in p16-positive aging cells aggravates high-fat diet-induced lung fibrosis by inhibiting NEDD4L-mediated K48-polyubiquitin-dependent degradation of SGK1.
Xin GuHaoyu MengChengyi PengShiyu LinBaihong LiLin ZhaoXue YangGuangyan WangWenyuan CaiJiawen ZhouShuiyuan LiuPeng WuYingqiang DuJianliang JinXiaoyan WangPublished in: Clinical and translational medicine (2023)
P16 accumulation promoted activation of integrin- inflammasome pathway and cell glycolysis by binding to the N- terminal of SGK1, intefering with the interaction between the E3 ubiquitin ligase NEDD4L and SGK1, thereby inhibiting K48- polyubiquitin- dependent degradation of SGK1 mediated by the NEDD4L-Ubch5 complex. ABT263 or EMD638683 could be used as potential drugs to treat pulmonary fibrosis in obese patients.
Keyphrases
- obese patients
- high fat diet induced
- pulmonary fibrosis
- bariatric surgery
- signaling pathway
- induced apoptosis
- insulin resistance
- roux en y gastric bypass
- gastric bypass
- single cell
- type diabetes
- cell therapy
- endoplasmic reticulum stress
- stem cells
- cell proliferation
- bone marrow
- oxidative stress
- drug induced
- cell migration