期刊
CELLS
卷 9, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/cells9061346
关键词
PLIN5; NAFLD; NASH; lipid droplets; NLRP3; inflammation; liver; hepatocytes; inflammasome; steatohepatitis
类别
资金
- German Research Foundation [SFB/TRR57, SFB 1052/Z3]
- Interdisciplinary Centre for Clinical Research within the Faculty of Medicine at the RWTH Aachen University (IZKF Aachen) [O3-1]
- P.U.R.E. (Protein Research Unit Ruhr within Europe), Ministry of Innovation, Science and Research of North-Rhine Westphalia, Germany
Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver diseases with an increasing prevalence due to rising rates of obesity, metabolic syndrome and type II diabetes. Untreated NAFLD may progress to steatohepatitis (NASH) and ultimately liver cirrhosis. NAFLD is characterized by lipid accumulation, and when sufficient excess lipids are obtained, irreversible liver injury may follow. Perilipin 5 (PLIN5), a known lipid droplet coating protein and triglyceride metabolism regulator, is highly expressed in oxidatively modified tissues but it is still unclear how it affects NAFLD/NASH progress. We here studied how PLIN5 affects NAFLD development induced by a 30-week high-fat diet (HFD) administration in wild type and PLIN5 knock out (Plin5(-/-)) mice. The disruption of PLIN5 induced differences in lipid metabolism during HFD feeding and was associated with reduced hepatic fat accumulation. Surprisingly,Plin5(-/-)mice showed mitigated activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome, leading to minor hepatic damage. We conclude that PLIN5 is a pleiotropic regulator of hepatic homeostasis in NASH development. Targeting the PLIN5 expression appears critical for protecting the liver from inflammatory activation during chronic NAFLD.
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