Lipoprotein(a) [Lp(a)] is a unique, genetically determined lipoprotein particle that has emerged as a significant independent risk factor for a wide spectrum of diseases beyond its well-established ro Show more
Lipoprotein(a) [Lp(a)] is a unique, genetically determined lipoprotein particle that has emerged as a significant independent risk factor for a wide spectrum of diseases beyond its well-established role in cardiovascular disease. Elevated Lp(a) levels are notoriously difficult to manage with conventional lipid-lowering therapies, posing a major clinical challenge. Recent advances have illuminated its complex pathophysiology, involving pro-inflammatory, pro-atherogenic, and pro-thrombotic pathways, which implicate Lp(a) in a diverse range of conditions including renal diseases, autoimmune disorders, and neurological conditions. Understanding the multifaceted role of Lp(a) across different organ systems is therefore of critical importance for developing targeted therapeutic strategies. A comprehensive synthesis of the evidence linking Lp(a) to these various pathologies is essential not only to consolidate our understanding of its mechanisms but also to identify patients at high risk across multiple disease domains. This review explores the molecular mechanisms by which Lp(a) contributes to disease pathogenesis, with a particular focus on inflammation and oxidative stress. We highlight the latest advances in novel, targeted therapeutic agents, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), which offer promising potential for specifically lowering Lp(a) levels. Furthermore, we discuss the implications of these therapies for modifying disease risk and improving clinical outcomes, offering hope for a paradigm shift in the management of Lp(a)-associated disorders. Show less
Cholesterol ester transfer protein (CETP) is responsible for the transformation of high density lipoprotein (HDL) to low density lipoprotein (LDL) and is a risk factor for atherosclerosis. Our study i Show more
Cholesterol ester transfer protein (CETP) is responsible for the transformation of high density lipoprotein (HDL) to low density lipoprotein (LDL) and is a risk factor for atherosclerosis. Our study investigated the association of the rs5883 CETP gene polymorphism with HDL and LDL levels, in 45 coronary artery disease patients and 45 control patients. CETP gene polymorphism was detected using Real Time-Polymerase Chain Reaction (RT-PCR). Lipoprotein levels were measured using Quantimetrix system. There were lack of associaition regarding CETP polymorphism in atherosclerosis and HDL and LDL levels (p>0.05) BMI was higher among coronary artery disease patients (CADP) compared to the control group (28.97±6.38, 26.52±4.39 respectively, p<0.03). Frequency of CADP (82.6 %, n=19) who were taking treatment was higher (17.4 %, n=4) (p<0.00). The frequencies of hypertension and type-2 diabetes were higher among CADP (p<0.00). Families of CADP have more CADP (p<0.02). Small HDL particle levels were higher in the control group (p<0.00). In Turkey, BMI, and frequencies of hypertension and type-2 diabetes were higher among CADP than among healthy controls. Furthermore, the genotypes of the rs5883 CETP gene polymorphism did not differ between CADP and healthy controls. Show less