Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India.
Program of Cardiovascular and Metabolic Disorders, Duke-NUS Medical School, 8 College Road, Singapore 169587, Singapore.
Int J Mol Sci. 2020 Mar 31;21(7):2391. doi: 10.3390/ijms21072391.
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors which belong to the nuclear hormone receptor superfamily. They regulate key aspects of energy metabolism within cells. Recently, PPARα has been implicated in the regulation of autophagy-lysosomal function, which plays a key role in cellular energy metabolism. PPARα transcriptionally upregulates several genes involved in the autophagy-lysosomal degradative pathway that participates in lipolysis of triglycerides within the hepatocytes. Interestingly, a reciprocal regulation of PPARα nuclear action by autophagy-lysosomal activity also exists with implications in lipid metabolism. This review succinctly discusses the unique relationship between PPARα nuclear action and lysosomal activity and explores its impact on hepatic lipid homeostasis under pathological conditions such as non-alcoholic fatty liver disease (NAFLD).
过氧化物酶体增殖物激活受体 (PPARs) 是配体激活的转录因子，属于核激素受体超家族。它们调节细胞内能量代谢的关键方面。最近，PPARα 被牵连到自噬溶酶体功能的调节中，自噬溶酶体功能在细胞能量代谢中起着关键作用。PPARα 转录上调了几个参与自噬溶酶体降解途径的基因，该途径参与肝细胞内甘油三酯的脂解。有趣的是，自噬溶酶体活性对 PPARα 核作用的反向调节也存在于脂代谢中。这篇综述简洁地讨论了 PPARα 核作用与溶酶体活性之间的独特关系，并探讨了其在非酒精性脂肪性肝病 (NAFLD) 等病理条件下对肝脂稳态的影响。
