The Role of Atherogenic Lipoproteins in Cardiovascular Diseases
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Lipids".
Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 404
Special Issue Editor
Interests: lysophosphatidylcholine; ceramide; lipoproteins; lipid metabolism; mitochondria dysfunction; atherosclerosis; cardiovascular diseases
Special Issue Information
Dear Colleagues,
Cardiovascular disease (CVD) remains the leading cause of death worldwide, and reducing the levels of low-density lipoprotein cholesterol (LDL-C) is the main objective of CVD therapy and secondary prevention. While medications such as statins and Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) inhibitors have been successful at reducing LDL-C levels, it is important to note that excessively low levels of LDL-C can increase the risk of all-cause mortality. Lipoproteins play a vital role in lipid transportation and metabolism. In animals, the genetic knockdown of apolipoprotein B100 (apoB100) or apolipoprotein E (apoE) leads to the early onset of various diseases.
For several decades, scientists have been studying modified lipoproteins such as oxidized LDL (oxLDL) and electronegative LDL (LDL(-)), as well as their signaling pathways. One of the most significant findings from this research is that these modified lipoproteins signal through the lectin-like oxidized LDL receptor-1 (LOX-1) to trigger vascular damage and the development of atherosclerosis. In this Special Issue, we present and discuss groundbreaking research on the high-throughput quantification of modified lipoproteins, in vivo evidence of atherosclerotic plaque formation, the pathogenesis of atherosclerosis, and innovative therapeutic strategies for tackling these modified lipoproteins.
Prof. Dr. Liang-Yin Ke
Guest Editor
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Keywords
- lysophosphatidylcholine (LPC)
- ceramide
- oxidized LDL (oxLDL)
- electronegative LDL (LDL(-))
- lectin-like oxidized LDL receptor-1 (LOX-1)
- lipid metabolism
- mitochondria dysfunction
- atherosclerosis
- cardiovascular diseases
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