The proprotein convertase subtilisin/kexin type 9 (PCSK9) was initially found to be involved in the regulation of apoptosis of neuronal cells and shortly thereafter emerged as a promising treatment target to lower serum cholesterol, a major risk factor of cardiovascular diseases. Only in the last few years, several breakthroughs in the understanding of PCSK9 biology have been reported illustrating how PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance.
This Research Topic will summarize experimental and clinical studies on PCSK9 and lipid metabolism including its regulation of the hepatic uptake of LDL-C by increasing the endosomal and lysosomal degradation of low-density lipoprotein (LDL) receptors (LDLR). Furthermore, it will focus on additional targets of PCSK9 which are also involved in lipid metabolisms such as the regulation of the very low-density lipoprotein receptor (VLDL), CD36 (cluster of differentiation 36) and the epithelial cholesterol transporter (NPC1L1), and its effects on the expression of apolipoprotein B48. Additionally, PCSK9 effects apart from lipid metabolism will be highlighted, since PCSK9 modifies function and survival of brain, cardiac and kidney cells.
We welcome articles on recent experimental and clinical data on PCSK9, the regulation of PCSK9, its extra-hepatic activities, the molecular concepts to target PCSK9. Recent clinical studies will also be reviewed and data will be summarized. We invite all authors to submit original data on PCSK9 related to the above topics.
The proprotein convertase subtilisin/kexin type 9 (PCSK9) was initially found to be involved in the regulation of apoptosis of neuronal cells and shortly thereafter emerged as a promising treatment target to lower serum cholesterol, a major risk factor of cardiovascular diseases. Only in the last few years, several breakthroughs in the understanding of PCSK9 biology have been reported illustrating how PCSK9 activity is tightly regulated at several levels by factors influencing its transcription, secretion, or by extracellular inactivation and clearance.
This Research Topic will summarize experimental and clinical studies on PCSK9 and lipid metabolism including its regulation of the hepatic uptake of LDL-C by increasing the endosomal and lysosomal degradation of low-density lipoprotein (LDL) receptors (LDLR). Furthermore, it will focus on additional targets of PCSK9 which are also involved in lipid metabolisms such as the regulation of the very low-density lipoprotein receptor (VLDL), CD36 (cluster of differentiation 36) and the epithelial cholesterol transporter (NPC1L1), and its effects on the expression of apolipoprotein B48. Additionally, PCSK9 effects apart from lipid metabolism will be highlighted, since PCSK9 modifies function and survival of brain, cardiac and kidney cells.
We welcome articles on recent experimental and clinical data on PCSK9, the regulation of PCSK9, its extra-hepatic activities, the molecular concepts to target PCSK9. Recent clinical studies will also be reviewed and data will be summarized. We invite all authors to submit original data on PCSK9 related to the above topics.
