The Different Facets of Dyslipidemia and Hypertension in Atherosclerosis.
Atherosclerosis is the narrowing of arteries due to the accumulation of macrophages overloaded with lipids resulting in foam cell formation, and these events occur preferentially at the branching points of arteries which are particularly susceptible to hyperlipidemic stress-induced inflammation and oxidative stress. The different stages of atherogenesis rely on oxidative stress, endothelial dysfunction, and inflammation, and hypertension or dyslipidemia can independently trigger these stages. Dyslipidemia and hypertension are pathological conditions that damage the endothelium, triggering cell proliferation, vascular remodeling, apoptosis, and increased cellular permeability with increased adhesion molecules that bind monocytes and T lymphocytes to create a vicious cocktail of pathophysiological factors. Correspondingly, the factors are redirected by chemo-attractants and pro-inflammatory cytokines into the intima of the vasculature, where monocytes differentiate into macrophages taking up oxidized LDL uncontrollably to form foam cells and atherosclerotic lesions. Moreover, endothelial damage also causes loss of vasomotor activity, disproportionate vascular contractility, and elevation of blood pressure in dyslipidemic patients, while in hypertensive patients, further elevation of blood pressure occurs, creating a self-perpetuating vicious cycle that aggravates the development and progression of atherosclerotic lesions. This review offers an in-depth analysis of atherosclerosis and the related interplay between dyslipidemia/hypertension and critically appraises the current diagnosis, etiology, and therapeutic options.
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Jessica
J
Hurtubise
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Krystie
K
McLellan
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Kevin
K
Durr
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Oluwadara
O
Onasanya
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada.
Daniel
D
Nwabuko
Department of Physiology, University of Saskatchewan College of Medicine, 107 Wiggins Road, Saskatoon, SK, S7N 5E5, Canada. joseph.ndisang@usask.ca.
Joseph Fomusi
JF
Ndisang
D000818:Animals; D050197:Atherosclerosis / Q000150:complications / Q000378:metabolism*; D050171:Dyslipidemias / Q000150:complications / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism; D008074:Lipoproteins / Q000378:metabolism; D018384:Oxidative Stress
D008074:Lipoproteins
Dyslipidemia; Endothelial dysfunction; High-density lipoprotein; Hypertension; Inflammation; Low-density lipoprotein; Oxidative stress