Lipoproteins, particularly low-density lipoprotein-like particles, including Lp(a), are causally involved in atherosclerosis. Our armamentarium to achieve intensive lipid-lowering has advanced considerably during the last decades, ranging from hydroxymethylglutaryl coenzyme A inhibition (statins), NPC1L1 blockage (ezetimibe), to specific PCSK9 inhibition, with newly emerging agents using monoclonal antibody- (e.g., evinacumab), antisense oligonucleotide- (e.g., vupanorsen, pelacarsen) or siRNA-based technologies (e.g., inclisiran, olpasiran) allowing for aggressive low-density lipoprotein cholesterol (LDL-C) lowering. Although these therapies open exciting avenues to further reduce adverse events, the residual cardiovascular risk remains substantial. Exemplified by a variety of landmark trials (e.g., FOURIER) showing that even if a marked LDL reduction is achieved, the overall event-rate remains high. Hence, the modification of quality rather than quantity might represent a promising avenue to address the huge burden of residual cardiovascular risk. While mechanisms linking native LDL-like particles and atherosclerosis have been investigated intensively, the mechanistic and/or therapeutic implications of other entities, such as dysfunctional HDL, Lp(a), modified LDL (oxidation, acetylation, glycosylation, carbamylation), LDL remnants, fatty acids, and oxidized phospholipids deserve focus. Advancing our understanding of the mechanisms linking modified lipid entities to atherogenesis may open novel diagnostic and therapeutic avenues to address the huge burden of residual cardiovascular risk.
This Research Topic will compile compelling articles ranging from original work, case reports, and editorials to state-of-the-art review articles, to eventually give the readership of Frontiers in Cardiovascular Medicine a neat overview of the role of lipids [Lp(a), non-HDL, fatty acids, oxidized phospholipids] modified lipoproteins [dysfunctional HDL, Lp(a), modified LDL, remnants] in different phases of atherogenesis. Indeed, this collection will not only deepen our understanding of mechanisms underpinning lesion formation but will also give an overview on recent forays toward their potential as novel diagnostic and therapeutic targets to successfully address the high burden of residual cardiovascular risk.
Led by an expert team of specialists, the Research Topic will accept manuscripts within this area of research, with the aim of giving the reader an overview of the latest discoveries and new findings, analysis of previously published data, new opinions and perspectives, and methods and protocols (when relevant).
Lipoproteins, particularly low-density lipoprotein-like particles, including Lp(a), are causally involved in atherosclerosis. Our armamentarium to achieve intensive lipid-lowering has advanced considerably during the last decades, ranging from hydroxymethylglutaryl coenzyme A inhibition (statins), NPC1L1 blockage (ezetimibe), to specific PCSK9 inhibition, with newly emerging agents using monoclonal antibody- (e.g., evinacumab), antisense oligonucleotide- (e.g., vupanorsen, pelacarsen) or siRNA-based technologies (e.g., inclisiran, olpasiran) allowing for aggressive low-density lipoprotein cholesterol (LDL-C) lowering. Although these therapies open exciting avenues to further reduce adverse events, the residual cardiovascular risk remains substantial. Exemplified by a variety of landmark trials (e.g., FOURIER) showing that even if a marked LDL reduction is achieved, the overall event-rate remains high. Hence, the modification of quality rather than quantity might represent a promising avenue to address the huge burden of residual cardiovascular risk. While mechanisms linking native LDL-like particles and atherosclerosis have been investigated intensively, the mechanistic and/or therapeutic implications of other entities, such as dysfunctional HDL, Lp(a), modified LDL (oxidation, acetylation, glycosylation, carbamylation), LDL remnants, fatty acids, and oxidized phospholipids deserve focus. Advancing our understanding of the mechanisms linking modified lipid entities to atherogenesis may open novel diagnostic and therapeutic avenues to address the huge burden of residual cardiovascular risk.
This Research Topic will compile compelling articles ranging from original work, case reports, and editorials to state-of-the-art review articles, to eventually give the readership of Frontiers in Cardiovascular Medicine a neat overview of the role of lipids [Lp(a), non-HDL, fatty acids, oxidized phospholipids] modified lipoproteins [dysfunctional HDL, Lp(a), modified LDL, remnants] in different phases of atherogenesis. Indeed, this collection will not only deepen our understanding of mechanisms underpinning lesion formation but will also give an overview on recent forays toward their potential as novel diagnostic and therapeutic targets to successfully address the high burden of residual cardiovascular risk.
Led by an expert team of specialists, the Research Topic will accept manuscripts within this area of research, with the aim of giving the reader an overview of the latest discoveries and new findings, analysis of previously published data, new opinions and perspectives, and methods and protocols (when relevant).