探讨TyG、SAA在动脉粥样硬化中的预测价值
To Investigate the Predictive Value of TyG and SAA in Atherosclerosis
DOI: 10.12677/ACM.2022.12111445, PDF,   
作者: 朱文举:青海大学,青海 西宁;左小芹:青海大学附属医院老年医学科,青海 西宁
关键词: 动脉粥样硬化TyGSAA心血管疾病炎症血管Atherosclerosis TyG SAA Cardiovascular Diseases Inflammation Vascular
摘要: 动脉粥样硬化是一种对人体危害较大的慢性心脑血管疾病;合并高血压、糖尿病除了导致下肢血管缺血跛行、下肢血管闭塞缺血性溃疡和截肢外,更重要的是这些患者心血管事件的风险明显增加,死亡率更高,主要死亡原因是心血管事件。脂代谢异常胰岛素抵抗和炎症反应导致血管内皮受损是动脉粥样硬化发生和发展的核心机制,不良生活习惯、年龄、糖尿病病程、血糖、血压、肥胖(尤其是腹型肥胖)、血脂、尿酸、环境污染物等,这些都加速动脉粥样硬化进展,导致肾功能减退和患者全因死亡风险增加显著,这篇综述阐述了导致动脉粥样硬化发生的影响因素及作用机制, 探讨了TyG、SAA在动脉粥样硬化中的潜在作用。
Abstract: Atherosclerosis is a kind of chronic cardio-cerebrovascular disease which is harmful to human body. In addition to lower extremity ischemic claudication, lower extremity vascular occlusive ischemic ulcers and amputation, these patients with hypertension and diabetes have a significantly in-creased risk of cardiovascular events and a higher mortality rate, and the main cause of death is cardiovascular events. Abnormal lipid metabolism insulin resistance and inflammation leading to vascular endothelial damage is the core mechanism of the occurrence and development of athero-sclerosis, bad living habits, age, diabetes course, blood sugar, blood pressure, obesity (especially abdominal obesity), lipid, uric acid, environmental pollutants, etc. These accelerate the progression of atherosclerosis, leading to renal decline and a significant increase in the risk of all-cause death in patients. This review describes the influencing factors and mechanism of atherosclerosis, and dis-cusses the potential role of TyG and SAA in atherosclerosis.
文章引用:朱文举, 左小芹. 探讨TyG、SAA在动脉粥样硬化中的预测价值[J]. 临床医学进展, 2022, 12(11): 10019-10025. https://doi.org/10.12677/ACM.2022.12111445

参考文献

[1] 褚现明, 李冰, 安毅, 等. 炎症与动脉粥样硬化关系研究进展[J]. 中国分子心脏病学杂志, 2010, 11(3): 184-188.
[2] Araujo, F. B., et al. (1995) Evaluation of Oxidative Stress in Patients with Hyperlipidemia. Atherosclero-sis, 117, 61-71. [Google Scholar] [CrossRef
[3] Farah, R., Shurtz-Swirski, R. and Dorlechter, F. (2010) Primed Polymorphonuclear Leukocytes Constitute a Possible Link between Inflammation and Oxidative Stress in Hyper-lipidemic Patients: Effect of Statins. Minerva Cardioangiologica, 58, 175-181.
[4] Lee, S.B., Ahn, C.W., Lee, B.K., et al. (2018) Association between Triglyceride Glucose Index and Arterial Stiffness in Korean Adults. Cardiovascular Di-abetology, 17, Article No. 41. [Google Scholar] [CrossRef] [PubMed]
[5] Wang, F., Han, L. and Hu, D. (2017) Fasting Insulin, Insulin Resistance and Risk of Hypertension in the General Population: A Meta-Analysis. Clinica Chimica Acta, 464, 57-63. [Google Scholar] [CrossRef] [PubMed]
[6] Lillioja, S., Mott, D.M., Spraul, M., et al. (1993) Insulin Resistance and Insulin Secretory Dysfunction as Precursors of Non-Insulin-Dependent Diabetes Mellitus: Prospective Studies of Pima Indians. The New England Journal of Medicine, 329, 1988-1992. [Google Scholar] [CrossRef
[7] Salonen, J.T., Lakka, T.A., Lakka, H.-M., Valkonen, V.-P., Everson, S.A. and Kaplan, G.A. (1998) Hyperinsulinemia Is Associated with the Incidence of Hypertension and Dyslipidemia in Middle-Aged Men. Diabetes, 47, 270-275. [Google Scholar] [CrossRef] [PubMed]
[8] Lee, E.Y., Yang, H.K., Lee, J., et al. (2016) Triglyceride Glucose Index, a Marker of Insulin Resistance, Is Associated with Coronary Artery Stenosis in Asymptomatic Subjects with Type 2 Di-abetes. Lipids in Health and Disease, 15, Article No. 155. [Google Scholar] [CrossRef] [PubMed]
[9] Mohd Nor, N.S., Lee, S., Bacha, F., Tfayli, H. and Arslanian, S. (2016) Triglyceride Glucose Index as a Surrogate Measure of Insulin Sensitivity in Obese Adolescents with Normoglycemia, Prediabetes, and Type 2 Diabetes Mellitus: Comparison with the Hyperinsulinemic-Euglycemic Clamp. Pediatric Diabetes, 17, 458-465. [Google Scholar] [CrossRef] [PubMed]
[10] Song, D.K., Lee, H., Sung, Y.-A. and Oh, J.-Y. (2016) Triglycerides to High-Density Lipoprotein Cholesterol Ratio Can Predict Impaired Glucose Tolerance in Young Women with Polycystic Ovary Syndrome. Yonsei Medical Journal, 57, 1404-1411. [Google Scholar] [CrossRef] [PubMed]
[11] Sanchez-Inigo, L., Navarro-Gonzalez, D., Fernandez-Montero, A., Pastrana-Delgado, J. and Martinez, J.A. (2016) The TyG Index May Predict the Development of Cardiovascular Events. European Journal of Clinical Investigation, 46, 189-197. [Google Scholar] [CrossRef] [PubMed]
[12] Eckel, R.H., Grundy, S.M. and Zimmet, P.Z. (2005) The Metabolic Syndrome. The Lancet, 365, 1415-1428. [Google Scholar] [CrossRef
[13] Bonora, E., Formentini, G., Calcaterra, F., et al. (2002) HOMA-Estimated Insulin Resistance Is an Independent Predictor of Cardiovascular Disease in Type 2 Diabetic Subjects: Prospective Data from the Verona Diabetes Complications Study. Diabetes Care, 25, 1135-1141. [Google Scholar] [CrossRef] [PubMed]
[14] Bressler, P., Bailey, S.R., Matsuda, M. and DeFronzo, R.A. (1996) Insulin Resistance and Coronary Artery Disease. Diabetologia, 39, 1345-1350. [Google Scholar] [CrossRef] [PubMed]
[15] Kim, M.K., Ahn, C.W., Kang, S., Nam, J.S., Kim, K.R. and Park, J.S. (2017) Relationship between the Triglyceride Glucose Index and Coronary Artery Calcification in Korean Adults. Cardi-ovascular Diabetology, 16, Article No. 108. [Google Scholar] [CrossRef] [PubMed]
[16] Simental-Mendia, L.E., Rodriguez-Moran, M. and Guerre-ro-Romero, F. (2008) The Product of Fasting Glucose and Triglycerides as Surrogate for Identifying Insulin Resistance in Apparently Healthy Subjects. Metabolic Syndrome and Related Disorders, 6, 299-304. [Google Scholar] [CrossRef] [PubMed]
[17] 张家庆. HOMA2-IR是一个较好的胰岛素抵抗指数[J]. 中华内分泌代谢杂志, 2005, 21(4): 304-305.
[18] De Fronzo, R.A. (2009) From the Triumvirate to the “Ominous Octet”: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus. Clinical Diabetology, 10, 101-128. [Google Scholar] [CrossRef] [PubMed]
[19] Mills, J.D. and Grant, P.J. (2002) Insulin Resistance, Haemostatic Factors and Cardiovascular Risk. The British Journal of Diabetes & Vascular Disease, 2, 19-26. [Google Scholar] [CrossRef
[20] Guerrero-Romero, F., Simental-Mendia, L.E., Gonza-lez-Ortiz, M., Martinez-Abundis, E., Ramos-Zavala, M.G., Hernandez-Gonzalez, S.O., et al. (2010) The Product of Tri-glycerides and Glucose, a Simple Measure of Insulin Sensitivity. Comparison with the Euglycemic-Hyperinsulinemic Clamp. The Journal of Clinical Endocrinology and Metabolism, 95, 3347-3351. [Google Scholar] [CrossRef] [PubMed]
[21] Sanchez-Inigo, L., Navarro-Gonzalez, D., Fernandez-Montero, A., Pas-trana-Delgado, J. and Martinez, J.A. (2016) The TyG Index May Predict the Development of Cardiovascular Events. European Journal of Clinical Investigation, 46, 189-197. [Google Scholar] [CrossRef] [PubMed]
[22] Ginsberg, H.N., Zhang, Y.L. and Hernandez-Ono, A. (2005) Regulation of Plasma Triglycerides in Insulin Resistance and Diabetes. Ar-chives of Medical Research, 36, 232-240. [Google Scholar] [CrossRef] [PubMed]
[23] Ma, M., Liu, H., Yu, J., He, S., Li, P., Ma, C., Zhang, H., Xu, L., Ping, F., Li, W., et al. (2020) Triglyceride Is Independently Correlated with Insulin Resistance and Islet Beta Cell Function: A Study in Population with Different Glucose and Lipid Metabolism States. Lipids in Health and Disease, 19, Article No. 121. [Google Scholar] [CrossRef] [PubMed]
[24] Lakatta, E.G. and Levy, D. (2003) Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: A “Set Up” for Vascular Disease. Circulation, 107, 139-146. [Google Scholar] [CrossRef
[25] Sengstock, D.M., Vaitkevicius, P.V. and Supiano, M.A. (2005) Arterial Stiffness Is Related to Insulin Resistance in Nondiabetic Hypertensive Older Adults. The Journal of Clinical Endocrinology & Metabolism, 90, 2823-2827. [Google Scholar] [CrossRef] [PubMed]
[26] Singh, R., Barden, A., Mori, T. and Beilin, L. (2001) Advanced Gly-cation End-Products: A Review. Diabetologia, 44, 129-146. [Google Scholar] [CrossRef] [PubMed]
[27] Arcaro, G., Cretti, A., Balzano, S., Lechi, A., Muggeo, M., Bonora, E. and Bonadonna, R.C. (2002) Insulin Causes Endothelial Dysfunction in Humans: Sites and Mechanisms. Circulation, 105, 576-582. [Google Scholar] [CrossRef] [PubMed]
[28] Yu, X., Wang, L., Zhang, W., Ming, J., Jia, A., Xu, S., et al. (2019) Fasting Tri-Glycerides and Glucose Index Is More Suitable for the Identification of Metabolically Unhealthy Individuals in the Chinese Adult Population: A Nationwide Study. Journal of Diabetes Investigation, 10, 1050e8.
[29] Maeda, M., Yamamoto, I., Fujio, Y., et al. (2003) Homocysteine Induces Vascular Endothelial Growth Factor Expression in Differ-entiated THP-1 Macrophages. Biochimica et Biophysica Acta, 1623, 41-46. [Google Scholar] [CrossRef
[30] 王则能, 颜彦. 肠道微生物与动脉粥样硬化[J]. 生命科学, 2017, 29(7): 682-686.
[31] Meek, R.L., Urieli-Shoval, S. and Benditt, E.P. (1994) Expression of Apolipoprotein Serum Amyloid A mRNA in Human Atherosclerotic Lesions and Cultured Vascular Cells: Implications for Serum Am-yloid A Function. Proceedings of the National Academy of Sciences of the United States of America, 91, 3186-3190. [Google Scholar] [CrossRef] [PubMed]
[32] O’Brien, K.D., McDonald, T.O., Kunjathoor, V., et al. (2005) Serum Amyloid A and Lipoprotein Retention in Murine Models of Atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 25, 785-790. [Google Scholar] [CrossRef
[33] Yamada, T., Kakihara, T., Kamishima, T., et al. (1996) Bothacutephase and Constitutive Serum Amyloid A Are Present in Atherosclerotic Lesions. Pathology International, 46, 797-800. [Google Scholar] [CrossRef] [PubMed]
[34] Dong, Z., Wu, T., Qin, W., et al. (2011) Serum Amyloid A Directly Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice. Molecular Medicine, 17, 1357-1364. [Google Scholar] [CrossRef] [PubMed]
[35] Thompson, J.C., Jayne, C., Thompson, J., et al. (2015) A Brief Elevation of Serum Amyloid A Is Sufficient to Increase Atherosclerosis. Journal of Lipid Research, 56, 286-293. [Google Scholar] [CrossRef
[36] Wilson, P.G., Thompson, J.C., Webb, N.R., et al. (2008) SAA, but Not CRP, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner. The American Journal of Pa-thology, 173, 1902-1910. [Google Scholar] [CrossRef] [PubMed]
[37] Boren, J. and Williams, K.J. (2016) The Central Role of Arterial Retention of Cholesterol-Rich Apolipoprotein-B-Containing Lipoproteins in the Pathogenesis of Atherosclerosis: A Tri-umph of Simplicity. Current Opinion in Lipidology, 27, 473-483. [Google Scholar] [CrossRef
[38] Krishack, P.A., Bhanvadia, C.V., Lukens, J., et al. (2015) Serum Amyloid A Facilitates Early Lesion Development in Ldlr-/-mice. Journal of the American Heart Association, 4, e001858. [Google Scholar] [CrossRef
[39] De Beer, M.C., Wroblewski, J.M., Noffsinger, V.P., et al. (2014) Deficiency of Endogenous Acute Phase Serum Amyloid A Does Not Affect Atherosclerotic Lesions in Apolipoprotein E-Deficient Mice. Arteriosclerosis, Thrombosis, and Vascular Biology, 34, 255-261. [Google Scholar] [CrossRef
[40] Thompson, J.C., Wilson, P.G., Shridas, P., et al. (2018) Se-rum Amyloid A3 Is Pro-Atherogenic. Atherosclerosis, 268, 32-35. [Google Scholar] [CrossRef] [PubMed]
[41] Lee, H.Y., Kim, S.D., Baek, S.H., et al. (2013) Serum Amyloid A Stimulates Macrophage Foam Cell Formation via Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Upregulation. Biochemical and Biophysical Research Communications, 433, 18-23. [Google Scholar] [CrossRef] [PubMed]
[42] 李骞. 瑞舒伐他汀对动脉粥样硬化大鼠SAA、hs-CRP的影响[D]: [硕士学位论文]. 福州: 福建医科大学, 2012.
[43] Sack, G.H. (2018) Serum Amyloid A—A Review. Molecu-lar Medicine, 24, Article No. 46. [Google Scholar] [CrossRef] [PubMed]
[44] Hoseini, Z., Sepahvand, F., Rashidi, B., et al. (2018) NLRP3 Inflammasome: Its Regulation and Involvement in Atherosclerosis. Journal of Cellular Physiology, 233, 2116-2132. [Google Scholar] [CrossRef] [PubMed]
[45] Shridas, P., De Beer, M.C. and Webb, N.R. (2018) High-Density Lipopro-tein Inhibits Serum Amyloid A-Mediated Reactive Oxygen Species Generation and NLRP3 Inflammasome Activation. Journal of Biological Chemistry, 293, 13257-13269. [Google Scholar] [CrossRef
[46] Webb, N.R., De Beer, M.C., Wroblewski, J.M., et al. (2015) Deficiency of Endogenous Acute-Phase Serum Amyloid A Protects ap-oE-/-mice from Angiotensin II-Induced Abdominal Aortic Aneurysm Formation. Arteriosclerosis, Thrombosis, and Vascular Biology, 35, 1156-1165. [Google Scholar] [CrossRef
[47] Madjid, M., Naghavi, M., Litovsky, S. and Casscells, S.W. (2003) Influenza and Cardiovascular Disease: A New Opportunity for Prevention and the Need for Further Studies. Circulation, 108, 2730-2736. [Google Scholar] [CrossRef
[48] Corrales-Medina, V.F., Madjid, M. and Musher, D.M. (2010) Role of Acute Infection in Triggering Acute Coronary Syndromes. The Lancet Infectious Diseases, 10, 83-92. [Google Scholar] [CrossRef
[49] Kaynar, A.M., Yende, S., Zhu, L., et al. (2014) Effects of Intra-Abdominal Sepsis on Atherosclerosis in Mice. Critical Care, 18, Article No. 469. [Google Scholar] [CrossRef] [PubMed]