Abstract
Atherosclerosis (AS) is a multifaceted inflammatory syndrome of the arterial wall to which number of mediators have been implicated in lesion progression. Triglyceride (TG)-rich lipoproteins consist of the large diversity of lipoprotein particles that fluctuate in density, size, and apolipoprotein composition. Two foremost phenotypes, on basis of size, chemical configuration, and density, of low-density-lipoprotein (LDL) have been recognized i.e., pattern A, having LDL diameter greater than 25.5nm (large buoyant LDL or lb-LDL) and pattern B, having LDL diameter less than or equal to 25.5nm (small-dense LDL or sd-LDL). Small-dense low-density-lipoprotein (sd-LDL) particles are produced by potential intravascular hydrolysis of TG-rich VLDL particles via lipoprotein lipases (LPLs), hepatic lipases (HLs) and cholesterol ester transfer protein (CETP). sd-LDL is more atherogenic due to its smaller size, increased penetration into the arterial wall, extended plasma half-life, lesser binding affinity for LDL receptors (LDL-R) as well as lower resistance to oxidative stress when equated with lb-LDL. The higher atherogenic potential of sd-LDL is due to its enhanced susceptibility to oxidation, owing to high polyunsaturated fatty acids (PUFA), low cholesterol and Apoprotein B (ApoB) content. An enhanced understanding of sd-LDL metabolism at the molecular level, transport and clearance may result in the development of sd-LDL as an independent predictive marker for AS events and may be used to maintain cholesterol homeostasis and prevent the succession of AS.
Highlights
Numerous pieces of evidence support the perception that the process of derangement between free radicals and antioxidants i.e., oxidative processes contribute to the pathogenesis of atherosclerosis (AS) and coronary heart disease (CHD)
Several risk factors contribute to the pathogenesis of AS i.e., hypertension, smoking, obesity, diabetes and dyslipidemia which is represented by increased triglycerides (TG), total and elevated low-density-lipoprotein (LDL) cholesterol levels, as well as decreased high-density lipoprotein (HDL) cholesterol [2,5,6]
It is known that loss of function mutations in proprotein convertase subtilisin/kexin type 9 (PCSK-9) showed increased LDL receptor (LDL-R) activity and diminished LDL levels in circulation though reverse is true with a gain of function mutations in PCSK-9 [108]
Summary
ABCG1: ATP-binding cassette sub-family G member 1 apo C-III: Apolipoproteins C-III. Numerous pieces of evidence support the perception that the process of derangement between free radicals and antioxidants i.e., oxidative processes contribute to the pathogenesis of atherosclerosis (AS) and coronary heart disease (CHD). Several risk factors contribute to the pathogenesis of AS i.e., hypertension, smoking, obesity, diabetes and dyslipidemia which is represented by increased triglycerides (TG), total and elevated low-density-lipoprotein (LDL) cholesterol levels, as well as decreased high-density lipoprotein (HDL) cholesterol [2,5,6]. High levels of LDL cholesterol have long been established as the most potent risk factors for coronary artery disease (CAD) [1,9,10,11]. Both normal and hyperlipidemic individuals showed differences in LDL size and size [12,13,14]. Therapeutic variability of different LDL subspecies is very helpful in decreasing the menace of cardiovascular events [14,15]
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