Atherosclerotic cardiovascular disease (ASCVD) remains one of the leading causes of morbidity and mortality worldwide. A large number of epidemiological and clinical studies have shown that dyslipidemia, especially the abnormal increase level of plasma low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG), is a key factor in the pathogenesis of ASCVD. Statins, one of the most famous lipids-lowering drugs, are still the first-line and cornerstone drugs for the prevention and treatment of ASCVD. Although statins can effectively reduce LDL-C, the reduction of TG is still unsatisfactory. Despite the chronicled successes from the use of statins, significant residual cardiovascular risk was still apparent in patients sufficiently compliant with statin treatment. At present, the most effective cholesterol-lowering drugs, statins and PCSK9 inhibitors, mainly accelerate the clearance of LDL-C in circulation by up-regulating hepatic LDL receptor (LDLR). There is still a lack of effective lipid-lowering drugs for patients with familial hypercholesterolemia, especially those who are completely deficient in LDLR, which remains the ultimate therapeutic challenge for lipidologists, cardiologists, and the pharmaceutical industry.
Different therapeutic targets for lowering lipids have been studied in pre-clinical and clinical studies, such as angiopoietin like protein 3 (ANGPTL3), apolipoprotein C3 (ApoC3), apolipoprotein B (ApoB), lipoprotein (a), and microsomal triglyceride transfer protein (MTTP). In the last two decades, ANGPTL3 has emerged as a novel therapeutic target for lowering all atherogenic lipoproteins independent of LDLR. Inhibition of ANGPTL3 dramatically reduces levels of both plasma LDL-C and TG in patients with or without heterozygous familial hypercholesterolemia (HeFH) who were refractory hypercholesterolemia. Here, we offer a platform for discussion, exchange, and updating our new insight into the molecular mechanism regulating lipid metabolism, exploring novel lipids-lowering targets. Research articles, reviews, case reports, editorials, and methodology papers that investigate and summarize the role of lipids metabolism in ASCVD and emerging lipid-lowering therapies are very welcome.
We welcome submissions on the following topics but are not limited to:
- New and emerging treatments for dyslipidemia and ASCVD
- Identification of new lipid-lowering compounds or targets
- Lipids-lowering therapy in patients with diabetes
- ANGPTL3 as a drug target in patients with diabetes
- Familial Hypercholesterolemia and lipoprotein(a)
- Apolipoproteins and ASCVD
- Triglyceride lowering therapy and ASCVD
- Combination lipid-lowering therapy
- Lipids-lowering therapy in women
Atherosclerotic cardiovascular disease (ASCVD) remains one of the leading causes of morbidity and mortality worldwide. A large number of epidemiological and clinical studies have shown that dyslipidemia, especially the abnormal increase level of plasma low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG), is a key factor in the pathogenesis of ASCVD. Statins, one of the most famous lipids-lowering drugs, are still the first-line and cornerstone drugs for the prevention and treatment of ASCVD. Although statins can effectively reduce LDL-C, the reduction of TG is still unsatisfactory. Despite the chronicled successes from the use of statins, significant residual cardiovascular risk was still apparent in patients sufficiently compliant with statin treatment. At present, the most effective cholesterol-lowering drugs, statins and PCSK9 inhibitors, mainly accelerate the clearance of LDL-C in circulation by up-regulating hepatic LDL receptor (LDLR). There is still a lack of effective lipid-lowering drugs for patients with familial hypercholesterolemia, especially those who are completely deficient in LDLR, which remains the ultimate therapeutic challenge for lipidologists, cardiologists, and the pharmaceutical industry.
Different therapeutic targets for lowering lipids have been studied in pre-clinical and clinical studies, such as angiopoietin like protein 3 (ANGPTL3), apolipoprotein C3 (ApoC3), apolipoprotein B (ApoB), lipoprotein (a), and microsomal triglyceride transfer protein (MTTP). In the last two decades, ANGPTL3 has emerged as a novel therapeutic target for lowering all atherogenic lipoproteins independent of LDLR. Inhibition of ANGPTL3 dramatically reduces levels of both plasma LDL-C and TG in patients with or without heterozygous familial hypercholesterolemia (HeFH) who were refractory hypercholesterolemia. Here, we offer a platform for discussion, exchange, and updating our new insight into the molecular mechanism regulating lipid metabolism, exploring novel lipids-lowering targets. Research articles, reviews, case reports, editorials, and methodology papers that investigate and summarize the role of lipids metabolism in ASCVD and emerging lipid-lowering therapies are very welcome.
We welcome submissions on the following topics but are not limited to:
- New and emerging treatments for dyslipidemia and ASCVD
- Identification of new lipid-lowering compounds or targets
- Lipids-lowering therapy in patients with diabetes
- ANGPTL3 as a drug target in patients with diabetes
- Familial Hypercholesterolemia and lipoprotein(a)
- Apolipoproteins and ASCVD
- Triglyceride lowering therapy and ASCVD
- Combination lipid-lowering therapy
- Lipids-lowering therapy in women