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1Nephrology Department, BP, A Beneficência Portuguesa de São Paulo, Brazil
2Intensive Care Unit, BP, A Beneficência Portuguesa de São Paulo, Brazil
*Corresponding author:Rocha Martinez TL, Nephrology Department, BP, A Beneficência Portuguesa de São Paulo, São Paulo, Brazil
Submission: March 31, 2022;Published: July 18, 2022<
ISSN: 2578-0204Volume3 Issue5
The growing interest in the mechanisms involved in atherogenesis is justifiable when it is verified that most of the deaths occurred in the Western world are due to ischemic syndromes related to atherosclerotic disease, that is, coronary insufficiency, cerebral vascular and peripherical vascular. The basis for formulating the lipid infiltration hypothesis for atherogenesis dates back to studies from the beginning of the century, when spontaneous atherosclerotic lesions in rabbit aortas were described. Ignatowiski and Anitshkow demonstrated that rabbits fed diets high in saturated fat and cholesterol developed atherosclerotic lesions in the aorta. Experimental studies “in vitro” and “in vivo”, using animal model, carried out in recent decades, which elucidated the properties of Low Density Lipoproteins (LDL) and their oxidative modifications, allowed a hypothesis to be proposed for the development of atheroma based on elevated LDL levels.
Keywords: Atherogenesis; Atherothrombotic lesion; Lipoproteins; Triglycerides Remnants; Lipoprotein(a)
Abbreviations: HDL: High Density Lipoprotein; HDL-c: High Density Lipoprotein Cholesterol; IDL: Intermediate Density Lipoprotein; LCAT: Lecithin Cholesterol Acyl Transferase; LDL: Low Density Lipoprotein; LDL-c: Low Density Lipoprotein Cholesterol; Lp(a): Lipoprotein(a); VLDL: Very Low Density Lipoprotein
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