전세계적으로 발병 및 사망률이 높은 동맥경화증은 뇌졸중, 심근경색 등 심혈관질환의 주요 병증의 원인인 만성 염

증성 질환이다. 동맥경화증은 지질 침착으로 인해 죽종(atheroma)이 형성되고, 혈전증이 유발되면서 관련 증상이 발생

한다. 동맥경화증의 합성 치료제의 부작용 우려로 인해 생물 유래 항동맥경화 소재 개발의 필요성이 강조되고 있다. 이

에 따라 동맥경화증의 개선 및 치료를 위한 바이오소재의 발굴 및 기전 규명 등 관련 연구가 활발히 수행되고 있다.

주로 동맥경화증 발병 관련 인자들을 조절하여 증상을 억제하거나 지연시키는 바이오소재들이 연구되고 있으며, 대표

적으로 다당류, 폴리페놀, 코엔자임 Q10이 해당된다. 우수한 활성을 가진 바이오소재의 경우에는 생체 내(동물 모델)

에서의 항동맥경화증 활성이 확인되었다. 본고에서는 동맥경화증의 발병 기전을 살펴보고, 항동맥경화증 활성이 보고

된 바이오소재의 연구 동향 및 활용 전망을 제시하고자 한다.

Atherosclerosis, a disease with high morbidity and mortality worldwide, is a chronic inflammatory disease

that is a major cause of cardiovascular diseases such as stroke and myocardial infarction. Atherosclerosis is characterized

by the accumulation of lipid deposits in the arteries, forming atheromas. This leads to the narrowing of the arteries and

thrombosis. Recently, the need to develop bio-derived anti-atherosclerotic materials has been highlighted with concerns

about the side effects of synthetic therapeutics. Accordingly, related research (such as the discovery of biomaterials for

the improvement and treatment of atherosclerosis and the identification of mechanisms) has been actively conducted.

Biomaterials including polysaccharides, polyphenols, and coenzyme Q10 have been reported to inhibit or delay symptoms

by modulating factors involved in the development of atherosclerosis. For biomaterials with superior activity, in vivo antiatherosclerotic

activity has been confirmed. In this review, the pathogenesis of atherosclerosis was investigated, and the

current status and application prospects of biomaterials with anti-atherosclerotic activity were proposed.

Atherosclerosis, Antioxidant, Biomaterial, Oxidative stress

1. Mc Namara, K., Alzubaidi, H. and Jackson, J. K., “Cardiovascular
Disease as a Leading Cause of Death: How Are Pharmacists
Getting Involved?,” Integr. Pharm. Res. Pract., 8, 1-11(2019).
2. Stewart, J., Manmathan, G. and Wilkinson, P., “Primary Prevention
of Cardiovascular Disease: A Review of Contemporary Guidance
and Literature,” Jrsm Cardiovasc. Dis., 6, 1-9(2017).
3. Kim, J. M., Lee, W. S. and Kim, J., “Therapeutic Strategy for Atherosclerosis
Based on Bone-vascular Axis Hypothesis,” Pharmacol.
Ther., 206, 107436(2020).
4. Steenman, M. and Lande, G., “Cardiac Aging and Heart Disease
in Humans,” Biophys. Rev., 9(2), 131-137(2017).
5. Mach, F., Ray, K. K., Wiklund, O., Corsini, A., Catapano, A. L.,
Bruckert, E., De Backer, G., Hegele, R. A., Hovingh, G.K. and
Jacobson, T.A., “Adverse Effects of Statin Therapy: Perception vs.
the Evidence–focus on Glucose Homeostasis, Cognitive, Renal
and Hepatic Function, Haemorrhagic Stroke and Cataract,” Eur.
Heart J., 39(27), 2526-2539(2018).
6. Volobueva, A., Zhang, D., Grechko, A. V. and Orekhov, A. N.,
“Foam Cell Formation and Cholesterol Trafficking and Metabolism
Disturbances in Atherosclerosis,” Cor Vasa, 61, 48-55(2018).
7. Michel, C. C. and Curry, F. E., “Microvascular Permeability,” Physiol.
Rev., 79, 703-761(1999).
8. Jang, E., Robert, J., Rohrer, L., von Eckardstein, A. and Lee, W.
L., “Transendothelial Transport of Lipoproteins,” Atherosclerosis,
315, 111-125(2020).
9. Vos, D. Y. and van de Sluis, B., “Function of the Endolysosomal
Network in Cholesterol Homeostasis and Metabolic-associatedFatty Liver Disease (MAFLD),” Mol. Metab., 50, 101146(2021).
10. Levitan, I., Volkov, S. and Subbaiah, P. V., “Oxidized LDL: Diversity,
Patterns of Recognition, and Pathophysiology,” Antioxid.
Redox Signal., 13(1), 39-75(2010).
11. Galimberti, F., Casula, M. and Olmastroni, E., “Apolipoprotein B
Compared with Low-density Lipoprotein Cholesterol in the Atherosclerotic
Cardiovascular Diseases Risk Assessment,” Pharmacol.
Res., 195, 106873(2023).
12. Ahmadi, A., Panahi, Y., Johnston, T. P. and Sahebkar, A., “Antidiabetic
Drugs and Oxidized Low-density Lipoprotein: A Review
of Anti-atherosclerotic Mechanisms,” Pharmacol. Res., 172, 105819
(2021).
13. Nachtigal, P., Semecky, V., Kopecky, M., Gojova, A., Solichova, D.,
Zdansky, P. and Zadak, Z., “Application of Stereological Methods
for the Quantification of VCAM-1 and ICAM-1 Expression
in Early Stages of Rabbit Atherogenesis,” Pathol. Res. Pract.,
200(3), 219-229(2004).
14. Lin, J., Kakkar, V. and Lu, X., “Impact of MCP-1 in Atherosclerosis,”
Curr. Pharm. Des., 20(28), 4580-4588(2014).
15. De Paoli, F., Staels, B. and Chinetti-Gbaguidi, G., “Macrophage
Phenotypes and Their Modulation in Atherosclerosis,” Circ. J., 78(8),
1775-1781(2014).
16. Hofnagel, O., Luechtenborg, B., Weissen-Plenz, G. and Robenek,
H., “Statins and Foam Cell Formation: Impact on LDL Oxidation
and Uptake of Oxidized Lipoproteins via Scavenger Receptors,”
Biochim. Biophys. Acta Mol. Cell Biol. Lipids, 1771(9), 1117-
1124(2007).
17. Chistiakov, D. A., Melnichenko, A. A., Myasoedova, V. A., Grechko,
A. V. and Orekhov, A. N., “Mechanisms of Foam Cell Formation
in Atherosclerosis,” J. Mol. Med., 95(11), 1153-1165(2017).
18. Williams, K. J. and Tabas, I., “Lipoprotein Retention-and Clues
for Atheroma Regression,” Arterioscler. Thromb. Vasc. Biol., 25(8),
1536-1540(2005).
19. Vlacil, A. K., Schuett, J., Schieffer, B. and Grote, K., “Variety
Matters: Diverse Functions of Monocyte Subtypes in Vascular
Inflammation and Atherogenesis,” Vasc. Pharmacol., 113, 9-19
(2019).
20. Nording, H., Baron, L. and Langer, H. F., “Platelets as Therapeutic
Targets to Prevent Atherosclerosis,” Atherosclerosis, 307, 97-
108(2020).
21. Mitra, S., Deshmukh, A., Sachdeva, R., Lu, J. and Mehta, J. L.,
“Oxidized Low-density Lipoprotein and Atherosclerosis Implications
in Antioxidant Therapy,” Am. J. Med. Sci., 342(2), 135-
142(2011).
22. Brown, R. A., Shantsila, E., Varma, C. and Lip, G. Y., “Current
Understanding of Atherogenesis,” Am. J. Med., 130(3), 268-282
(2017).
23. Maguire, E. M., Pearce, S. W. and Xiao, Q., “Foam Cell Formation:
A New Target for Fighting Atherosclerosis and Cardiovascular
Disease,” Vascul. Pharmacol., 112, 54-71(2019).
24. Yan, P., Xia, C., Duan, C., Li, S. and Mei, Z., “Biological Characteristics
of Foam Cell Formation in Smooth Muscle Cells
Derived From Bone Marrow Stem Cells,” Int. J. Biol. Sci., 7(7),
937(2011).
25. Sorokin, V., Vickneson, K., Kofidis, T., Woo, C. C., Lin, X. Y.,
Foo, R. and Shanahan, C. M., “Role of Vascular Smooth Muscle
Cell Plasticity and Interactions in Vessel Wall Inflammation,”
Front. immunol., 11, 599415(2020).
26. Sanson, M., Augé, N., Vindis, C., Muller, C., Bando, Y., Thiers,
J. C., Marachet, M. A., Zarkovic, K., Sawa, Y., Salvayre, R. and
Nègre-Salvayre, A., “Oxidized Low-density Lipoproteins Trigger
Endoplasmic Reticulum Stress in Vascular Cells: Prevention by
Oxygen-regulated Protein 150 Expression,” Circ. Res., 104(3),
328-336(2009).
27. Cheng, H., Cheng, Q., Bao, X., Luo, Y., Zhou, Y., Li, Y., Hua,
Q., Liu, W., Tang, S. Feng, D. and Luo, Z., “Over-activation of
NMDA Receptors Promotes ABCA1 Degradation and Foam
Cell Formation,” Biochim. Biophys. Acta Mol. Cell Biol. Lipids,
1865(10), 158778(2020).
28. Teng, N., Maghzal, G. J., Talib, J., Rashid, I., Lau, A. K. and Stocker,
R., “The Roles of Myeloperoxidase in Coronary Artery Disease
and Its Potential Implication in Plaque Rupture,” Redox Rep., 22(2),
51-73(2017).
29. Bentzon, J. F., Otsuka, F., Virmani, R. and Falk, E., “Mechanisms
of Plaque Formation and Rupture,” Circ. Res., 114(12), 1852-
1866(2014).
30. Watson, M. G., Byrne, H. M., Macaskill, C. and Myerscough, M.
R., “A Two-phase Model of Early Fibrous Cap Formation in
Atherosclerosis,” J. Theor. Biol., 456, 123-136(2018).
31. Glass, C. K. and Witztum, J. L. Atherosclerosis: the Road Ahead.
Cell, 104(4), 503-516(2001).
32. Huang, N. F., Okogbaa, J., Lee, J. C., Jha, A., Zaitseva, T. S.,
Paukshto, M. V., Sun, J. S., Punjya, N., Fuller, G. G. and Cooke,
J. P., “The Modulation of Endothelial Cell Morphology, Function,
and Survival Using Anisotropic Nanofibrillar Collagen Scaffolds,”
Biomaterials, 34(16), 4038-4047(2013).
33. Cameron, J. N., Mehta, O. H., Michail, M., Chan, J., Nicholls, S.
J., Bennett, M. R. and Brown, A. J., “Exploring the Relationship
Between Biomechanical Stresses and Coronary Atherosclerosis,”
Atherosclerosis, 302, 43-51(2020).
34. Chien, S., “Molecular and Mechanical Bases of Focal Lipid
Accumulation in Arterial Wall,” Prog. Biophys. Mol., 83(2), 131-
151(2003).
35. Chiu, J. J., Lee, P. L., Chen, C. N., Lee, C. I., Chang, S. F., Chen,
L. J., Lien, S. C., Ko., Y. C., Usami, S. and Chien, S., “Shear
Stress Increases ICAM-1 and Decreases VCAM-1 and E-selectin
Expressions Induced by Tumor Necrosis Factor-α in Endothelial
Cells,” Arter. Thromb. Vasc. Biol., 24(1), 73-79(2004).
36. Zhou, M., Yu, Y., Chen, R., Liu, X., Hu, Y., Ma, Z., Gao, L., Jian,
W. and Wang, L. “Wall Shear Stress and Its Role in Atherosclerosis,”
Front. Cardiovasc. Med., 10, 1083547(2023).
37. Williams, H., Johnson, J. L., Jackson, C. L., White, S. J. and George,
S. J., “MMP-7 Mediates Cleavage of N-cadherin and Promotes
Smooth Muscle Cell Apoptosis,” Cardiovasc. Res., 87(1), 137-
146(2010).
38. Newby, A. C., “Proteinases and Plaque Rupture: Unblocking the
Road to Translation,” Curr. Opin. Lipidol., 25(5), 358-366(2014).
39. Barascuk, N., Skjøt-Arkil, H., Register, T. C., Larsen, L., Byrjalsen,
I., Christiansen, C. and Karsdal, M. A., “Human Macrophage
Foam Cells Degrade Atherosclerotic Plaques Through
Cathepsin K Mediated Processes,” BMC Cardiovasc. Disord., 10(1),
1-9(2010).
40. Luo, P. and Qiu, B., “The Role of Immune Cells in Pulmonary
Hypertension: Focusing on Macrophages,” Hum. Immunol., 83(2),153-163(2022).
41. Wen, G., Zhang, C., Chen, Q., Mustafa, A., Ye, S. and Xiao, Q.,
“A Novel Role of Matrix Metalloproteinase-8 in Macrophage
Differentiation and Polarization,” J. Biol. Chem., 290(31), 19158-
19172(2015).
42. Liu, J., Guo, Z., Zhang, Y., Wu, T., Ma, Y., Lai, W. and Guo, Z.,
“LCK Inhibitor Attenuates Atherosclerosis in ApoE-/- mice via
Regulating T Cell Differentiation and Reverse Cholesterol Transport,”
J. Mol. Cell. Cardiol., 139, 87-97(2020).
43. Yan, A. and Gotlieb, A. I., “The Microenvironment of the Atheroma
Expresses Phenotypes of Plaque Instability,” Cardiovasc.
Pathol., 107572(2023).
44. Goikuria, H., Vandenbroeck, K. and Alloza, I., “Inflammation in
Human Carotid Atheroma Plaques,” Cytokine Growth Factor
Rev., 39, 62-70(2018).
45. Camaré, C., Pucelle, M., Nègre-Salvayre, A. and Salvayre, R.,
“Angiogenesis in the Atherosclerotic Plaque,” Redox Biol., 12,
18-34(2017).
46. Perrotta, P., Veseli, B. E., Van der Veken, B., Roth, L., Martinet,
W. and De Meyer, G. R., “Pharmacological Strategies to Inhibit
Intra-plaque Angiogenesis in Atherosclerosis,” Vasc. Pharmacol.,
112, 72-78(2019).
47. Moreno, P. R., Purushothaman, M. and Purushothaman, K. R.,
“Plaque Neovascularization: Defense Mechanisms, Betrayal, or
a War in Progress,” Ann. N. Y. Acad. Sci., 1254(1), 7-17(2012).
48. van Eif, V. W., Devalla, H. D., Boink, G. J. and Christoffels, V.
M., “Transcriptional Regulation of the Cardiac Conduction System,”
Nat. Rev. Cardiol., 15(10), 617-630(2018).
49. Lu, D. and Thum, T., “RNA-based Diagnostic and Therapeutic
Strategies for Cardiovascular Disease,” Nat. Rev. Cardiol., 16(11),
661-674(2019).
50. Wang, Y., Chen, Y., Zhang, X., Lu, Y. and Chen, H., “New
Insights in Intestinal Oxidative Stress Damage and the Health
Intervention Effects of Nutrients: A Review,” J. Funct. Food.,
75, 104248(2020).
51. Ighodaro, O. M. and Akinloye, O. A., “First Line Defence Antioxidants-superoxide
Dismutase (SOD), Catalase (CAT) and Glutathione
Peroxidase (GPX): Their Fundamental Role in the Entire
Antioxidant Defence Grid,” Alex. J. Med., 54(4), 287-293(2018).
52. Jo, J., Shin, S., Jung, H., Min, B., Kim, S. and Kim, J., “Process
Development for Production of Antioxidants from Lipid Extracted
Microalgae Using Ultrasonic-assisted Extraction,” Korean Chem.
Eng. Res., 55(4), 542-547(2017).
53. Min, B., Han, Y., Lee, D., Jo, J., Jung, H. and Kim, J. W., “Optimization
of Microwave-assisted Extraction Conditions for Production
of Bioactive Material from Corn Stover,” Korean Chem.
Eng. Res., 56(1), 66-72(2018).
54. Pisoschi, A. M., Pop, A., Iordache, F., Stanca, L., Predoi, G. and
Serban, A. I., “Oxidative Stress Mitigation by Antioxidants-an
Overview on Their Chemistry and Influences on Health Status,”
Eur. J. Med. Chem., 209, 112891(2020).
55. Fallah, A. A., Sarmast, E. and Jafari, T. “Effect of Dietary Anthocyanins
on Biomarkers of Oxidative Stress and Antioxidative Capacity:
A Systematic Review and Meta-analysis of Randomized Controlled
Trials,” J. Funct. Food., 68, 103912(2020).
56. Daiber, A. and Chlopicki, S., “Revisiting Pharmacology of Oxidative
Stress and Endothelial Dysfunction in Cardiovascular
Disease: Evidence for Redox-based Therapies,” Free Radic. Biol.
Med., 157, 15-37(2020).
57. Yalameha, B., “Antioxidant Therapy to Improve or Resolve Atherosclerosis;
New Hopes and Current Trends,” J. Nephropharmacology,
8(2), e18-e18(2019).
58. Yoshida, H. and Kisugi, R., “Mechanisms of LDL Oxidation,”
Clin. Chim. Acta, 411(23-24), 1875-1882(2010).
59. Cyr, A. R., Huckaby, L. V., Shiva, S. S. and Zuckerbraun, B. S.,
“Nitric Oxide and Endothelial Dysfunction,” Crit. Care Clin.,
36(2), 307-321(2020).
60. Frombaum, M., Le Clanche, S., Bonnefont-Rousselot, D. and
Borderie, D., “Antioxidant Effects of Resveratrol and Other Stilbene
Derivatives on Oxidative Stress and NO Bioavailability: Potential
Benefits to Cardiovascular Diseases,” Biochimie, 94(2), 269-276
(2012).
61. Gradinaru, D., Borsa, C., Ionescu, C. and Prada, G. I., “Oxidized
LDL and NO Synthesis-biomarkers of Endothelial Dysfunction
and Ageing,” Mech. Ageing Dev., 151, 101-113(2015).
62. Yang, X., Li, Y., Li, Y., Ren, X., Zhang, X., Hu, D., Gao, Y., Xing, Y.
and Shang, H., “Oxidative Stress-mediated Atherosclerosis: Mechanisms
and Therapies,” Front. Physiol. 8, 600(2017).
63. Schleicher, E. and Friess, U., “Oxidative Stress, AGE, and Atherosclerosis,”
Kidney Int., 72, S17-S26(2007).
64. Lee, M., Oh, S., Chu, C. H., Kim, Y. S., Na, I. C. and Park, K.,
“Enhancement of Membrane Durability in PEMFC by Fucoidan
and Tannic Acid,” Korean Chem. Eng. Res., 61(1), 45-51(2023).
65. Zayed, A. and Ulber, R., “Fucoidan Production: Approval Key
Challenges and Opportunities,” Carbohydr. Polym., 211, 289-297
(2019).
66. Pradhan, B., Patra, S., Nayak, R., Behera, C., Dash, S. R., Nayak,
S., Sahu, B. B. and Jena, M., “Multifunctional Role of Fucoidan,
Sulfated Polysaccharides in Human Health and Disease: A Journey
Under the Sea in Pursuit of Potent Therapeutic Agents,” Int.
J. Biol. Macromol., 164, 4263-4278(2020).
67. Mansour, M. B., Balti, R., Yacoubi, L., Ollivier, V., Chaubet, F.
and Maaroufi, R. M., “Primary Structure and Anticoagulant Activity
of Fucoidan From the Sea Cucumber Holothuria polii. Int. J.
Biol. Macromol., 121, 1145-1153(2019).
68. Pozharitskaya, O. N., Obluchinskaya, E. D. and Shikov, A. N.,
“Mechanisms of Bioactivities of Fucoidan From the Brown Seaweed
Fucus vesiculosus L. of the Barents Sea,” Mar. Drugs, 18(5), 275
(2020).
69. Dutot, M., Grassin-Delyle, S., Salvator, H., Brollo, M., Rat, P., Fagon,
R., Naline, E. and Devillier, P., “A Marine-sourced Fucoidan
Solution Inhibits Toll-like-receptor-3-induced Cytokine Release
by Human Bronchial Epithelial Cells,” Int. J. Biol. Macromol.,
130, 429-436(2019).
70. Yin, J., Wang, J., Li, F., Yang, Z., Yang, X., Sun, W., Xia, B., Li,
T., Song, W. and Guo, S., “The Fucoidan From the Brown Seaweed
Ascophyllum nodosum Ameliorates Atherosclerosis in Apolipoprotein
E-deficient Mice,” Food Funct., 10(8), 5124-5139(2019).
71. Novoyatleva, T., Kojonazarov, B., Owczarek, A., Veeroju, S., Rai,
N., Henneke, I., Bohm, M., Grimminger, F., Ghofrani, H. A.,
Seeger, W., Weissmann, N. and Schermuly, R. T. “Evidence for the
Fucoidan/P-selectin Axis as a Therapeutic Target in Hypoxiainduced
Pulmonary Hypertension,” Am. J. Respir. Crit. Care
Med., 199(11), 1407-1420(2019).72. Jayachandran, M., Chen, J., Chung, S. S. M. and Xu, B. “A Critical
Review on the Impacts of β-glucans on Gut Microbiota and
Human Health,” J. Nutr. Biochem., 61, 101-110(2018).
73. Bai, J., Ren, Y., Li, Y., Fan, M., Qian, H., Wang, L., Wu, G.,
Zhang, H., Qi, X., Xu, M. and Rao, Z., “Physiological Functionalities
and Mechanisms of β-glucans,” Trends Food Sci. Technol.,
88, 57-66(2019).
74. Gislette, T., Zhao, K. N., Gu, W. and Chen, J., “The Possible
Mechanisms for β-glucans to Prevent Atherosclerotic Lesions,”
Curr. Bioact. Compd., 8(2), 146-150(2012).
75. Wang, S., Zhou, H., Feng, T., Wu, R., Sun, X., Guan, N., Qu, L.,
Gao, Z., Yan, J., Nu, N. and Zhao, J., “β-glucan Attenuates
Inflammatory Responses in Oxidized LDL-induced THP-1 Cells
via the p38 MAPK Pathway,” Nutr. Metab. Cardiovasc. Dis.,
24(3), 248-255(2014).
76. Aoki, S., Iwai, A., Kawata, K., Muramatsu, D., Uchiyama, H.,
Okabe, M., Ikesue, M., Maeda, N. and Uede, T., “Oral Administration
of the β-glucan Produced by Aureobasidium pullulans
Ameliorates Development of Atherosclerosis in Apolipoprotein
E Deficient Mice,” J. Funct. Foods, 18, 22-27(2015).
77. Jiang, Y., Fu, C., Liu, G., Guo, J. and Su, Z., “Cholesterol-lowering
Effects and Potential Mechanisms of Chitooligosaccharide Capsules
in Hyperlipidemic Rats,” Food Nutr. Res., 62(2018).
78. Liang, S., Sun, Y. and Dai, X., “A Review of the Preparation, Analysis
and Biological Functions of Chitooligosaccharide,” Int. J.
Mol. Sci., 19(8), 2197(2018).
79. Yang, D., Hu, C., Deng, X., Bai, Y., Cao, H., Guo, J. and Su, Z.
Therapeutic Effect of Chitooligosaccharide Tablets on Lipids in
High-fat Diets Induced Hyperlipidemic Rats,” Molecules, 24(3),
514(2019).
80. Kang, N. H., Lee, W. K., Yi, B. R., Lee, H. R., Park, M. A., Park, S.
K., Park, H. K. and Choi, K. C., “Risk of Cardiovascular Disease is
Suppressed by Dietary Supplementation with Protamine and Chitooligosaccharide
in Sprague-Dawley Rats,” Mol. Med. Rep., 7(1),
127-133(2013).
81. Phil, L., Naveed, M., Mohammad, I. S., Bo, L. and Bin, D.,
“Chitooligosaccharide: An Evaluation of Physicochemical and
Biological Properties with the Proposition for Determination of
Thermal Degradation Products,” Biomed. Pharmacother., 102,
438-451(2018).
82. Isemura, M., “Catechin in Human Health and Disease,” Molecules,
24(3), 528(2019).
83. Miura, Y., Chiba, T., Tomita, I., Koizumi, H., Miura, S., Umegaki,
K., Hara, Y. and Ikeda, M., “Tea Catechins Prevent the Development
of Atherosclerosis in Apoprotein E-deficient Mice,” J. Nutr.,
131(1), 27-32(2001).
84. Suzuki, J. I., Isobe, M., Morishita, R. and Nagai, R., “Tea Polyphenols
Regulate Key Mediators on Inflammatory Cardiovascular
Diseases,” Mediat. Inflamm., 2009, 494928(2009).
85. Malekmohammad, K., Sewell, R. D. and Rafieian-Kopaei, M.,
“Antioxidants and Atherosclerosis: Mechanistic Aspects,” Biomolecules,
9(8), 301(2019).
86. Risuleo, G., in Gupta, R. C.(Ed.), Resveratrol: Multiple Activities
on the Biological Functionality of the Cell. Academic Press,
Boston, MA, USA, 453-464(2016).
87. Poznyak, A. V., Grechko, A. V., Orekhova, V. A., Chegodaev, Y.
S., Wu, W. K. and Orekhov, A. N., “Oxidative Stress and Antioxidants
in Atherosclerosis Development and Treatment,” Biology,
9(3), 60(2020).
88. Zhou, L., Long, J., Sun, Y., Chen, W., Qiu, R. and Yuan, D., “Resveratrol
Ameliorates Atherosclerosis Induced by High-fat Diet
and LPS in ApoE-/- Mice and Inhibits the Activation of CD4+
T
Cells,” Nutr. Metab., 17, 1-12(2020).
89. Figueira, L. and González, J. C., “Effect of Resveratrol on Seric
Vascular Endothelial Growth Factor Concentrations During Atherosclerosis,”
Clin. Invest. Arterioscler., 30(5), 209-216(2018).
90. Bonakdar, R. A. and Guarneri, E., “Coenzyme Q10,” Am. Fam.
Physician, 72(6), 1065-1070(2005).
91. Flowers, N., Hartley, L., Todkill, D., Stranges, S. and Rees, K.,
“Co-enzyme Q10 Supplementation for the Primary Prevention
of Cardiovascular Disease,” Cochrane Database Syst Rev., (12),
CD010405(2014).
92. Ulla, A., Mohamed, M. K., Sikder, B., Rahman, A. T., Sumi, F.
A., Hossain, M. Reza, H. M., Rahman, G. M. S. and Alam, M.
A., “Coenzyme Q10 Prevents Oxidative Stress and Fibrosis in
Isoprenaline Induced Cardiac Remodeling in Aged Rats,” BMC
Pharmacol. Toxicol., 18(1), 1-10(2017).
93. Dludla, P. V., Nyambuya, T. M., Orlando, P., Silvestri, S., Mxinwa,
V., Mokgalaboni, K., Nkambule, B. B., Louw, J., Muller, C. J. F.
and Tiano, L., “The Impact of Coenzyme Q10 on Metabolic and
Cardiovascular Disease Profiles in Diabetic Patients: A Systematic
Review and Meta-analysis of Randomized Controlled Trials,”
Endocrinol. Diabetes Metab., 3, e00118(2020).