A Comprehensive Review of Oxidative Stress as the Underlying Mechanism in Atherosclerosis and the Inefficiency of Antioxidants to Revert this Process

被引:6
作者
Cabezas, Kevin G. [1 ]
Gomez-Fernandez, Carmen R. [2 ]
Vazquez-Padron, Roberto [1 ]
机构
[1] UMMSM, Dept Vasc Surg & Endovasc Surg, 1600 NW 10th Ave 1140, Miami, FL 33136 USA
[2] UMMSM, Univ Miami Hosp Pathol & Lab Med, 1600 NW 10th Ave 1140, Miami, FL 33136 USA
关键词
Atherosclerosis; reactive oxygen species; oxidative stress; antioxidants; cardiovascular diseases; chronic disease; KAPPA-B; PROTEIN-1; APOPTOSIS; RECEPTORS; VCAM-1; CELLS;
D O I
10.2174/1381612825666190116103323
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background: Cardiovascular diseases account for the highest mortality rate in the United States. The major underlying mechanism driving the onset and maintenance of cardiovascular diseases is atherosclerosis. Atherosclerosis is a chronic disease affecting large and medium-size arteries; it proceeds through four main stages along different decades of life, beginning at birth. Atherosclerosis is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted. Failure of intrinsic antioxidants and prophylactic antioxidant supplements to prevent atherosclerosis formation is an ongoing area of research in the race to avert, manage and cure atherosclerosis. Methods: The purpose of this work was to elucidate the actions of reactive oxygen species and oxidative stress on the formation of atherosclerosis as well as the different stages of atherosclerosis and the different mechanisms to prevent it. Through an extensive review of scientific literature, this paper correlates cell damage caused by oxidative stress to atheromatous plaque formation, as well as an in-depth analysis of high-density lipoproteins and enzymatic and non-enzymatic antioxidant role on atherosclerosis prevention. The antioxidant mechanism is overwhelmed by atherosclerotic processes and fails to be the ideal treatment of atherosclerosis. There is no scientific data that correlates prophylactic and non-prophylactic antioxidant treatment to a decrease in mortality or comorbidities pertaining to atherosclerosis. This is thought to be due to lack of consensus of optimal therapeutic doses, lack of reliable markers indicating which patient is to benefit from therapy and the chemical complexity of antioxidants in vivo. Current treatments for atherosclerosis include HMG-CoA reductase inhibitors which directly target low-density lipoproteins to tackle atherosclerotic plaque formation. Conclusion: HMG-CoA reductase inhibitors are not enough for the treatment of atherosclerosis given the complexity of the disease which has immune, musculoskeletal, genetic and hematologic aspects besides the involvement of lipids and lipoproteins. Therefore, other pharmacologic targets such as the PCSK9 enzyme and NFK-beta should be researched in depth as possible treatments for atherosclerosis.
引用
收藏
页码:4705 / 4710
页数:6
相关论文
共 35 条
[1]   High-Density Lipoprotein and Atherosclerosis: The Role of Antioxidant Activity [J].
Bandeali, Salman ;
Farmer, John .
CURRENT ATHEROSCLEROSIS REPORTS, 2012, 14 (02) :101-107
[2]   Nitric oxide - the endothelium-derived relaxing factor and its role in endothelial functions [J].
Bauer, Viktor ;
Sotnikova, Ruzena .
GENERAL PHYSIOLOGY AND BIOPHYSICS, 2010, 29 (04) :319-340
[3]   Reactive oxygen species [J].
Bayir, H .
CRITICAL CARE MEDICINE, 2005, 33 (12) :S498-S501
[4]   Apoptosis in the cardiovascular system [J].
Bennett, MR .
HEART, 2002, 87 (05) :480-487
[5]   Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis [J].
Bobryshev, Yuri V. ;
Ivanova, Ekaterina A. ;
Chistiakov, Dimitry A. ;
Nikiforov, Nikita G. ;
Orekhov, Alexander N. .
BIOMED RESEARCH INTERNATIONAL, 2016, 2016
[6]   Angiotensin II stimulates matrix metalloproteinase secretion in human vascular smooth muscle cells via nuclear factor-κB and activator protein 1 in a redox-sensitive manner [J].
Browatzki, M ;
Larsen, D ;
Pfeiffer, CAH ;
Gehrke, SG ;
Schmidt, J ;
Kranzhöfer, A ;
Katus, HA ;
Kranzhöfer, R .
JOURNAL OF VASCULAR RESEARCH, 2005, 42 (05) :415-423
[7]   Mechanisms of foam cell formation in atherosclerosis [J].
Chistiakov, Dimitry A. ;
Melnichenko, Alexandra A. ;
Myasoedova, Veronika A. ;
Grechko, Andrey V. ;
Orekhov, Alexander N. .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2017, 95 (11) :1153-1165
[8]   MINIMALLY MODIFIED LOW-DENSITY-LIPOPROTEIN INDUCES MONOCYTE CHEMOTACTIC PROTEIN-1 IN HUMAN ENDOTHELIAL-CELLS AND SMOOTH-MUSCLE CELLS [J].
CUSHING, SD ;
BERLINER, JA ;
VALENTE, AJ ;
TERRITO, MC ;
NAVAB, M ;
PARHAMI, F ;
GERRITY, R ;
SCHWARTZ, CJ ;
FOGELMAN, AM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (13) :5134-5138
[9]  
Das U N, 2005, J Assoc Physicians India, V53, P472
[10]  
Declercq W, 1998, J IMMUNOL, V161, P390