Int J Angiol 2022; 31(01): 001-009
DOI: 10.1055/s-0042-1742587
Review Article

Does AGE–RAGE Stress Play a Role in the Development of Coronary Artery Disease in Obesity?

Kailash Prasad
1   Department of Physiology (APP), College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
,
Amal S. Khan
2   Community, Health and Epidemiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
,
Kalpana K. Bhanumathy
3   Division of Oncology, Cancer Cluster Unit, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
› Author Affiliations

Abstract

This article deals with the role of AGE (advanced glycation end products)–RAGE (receptor for AGE) stress (AGE/sRAGE) in the development of coronary artery disease (CAD) in obesity. CAD is due to atherosclerosis in coronary artery. The serum/plasma levels of AGE and sRAGE are reduced, while AGE–RAGE stress and expression of RAGE are elevated in obese individuals. However, the levels of AGE are elevated in obese individuals with more than one metabolic syndrome. The increases in the AGE–RAGE stress would elevate the expression and production of atherogenic factors, including reactive oxygen species, nuclear factor-kappa B, cytokines, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial leukocyte adhesion molecules, monocyte chemoattractant protein-1, granulocyte-macrophage colony-stimulating factor, and growth factors. Low levels of sRAGE would also increase the atherogenic factors. The increases in the AGE–RAGE stress and decreases in the levels of sRAGE would induce development of atherosclerosis, leading to CAD. The therapeutic regimen for AGE–RAGE stress–induced CAD in obesity would include lowering of AGE intake, prevention of AGE formation, degradation of AGE in vivo, suppression of RAGE expression, blockade of AGE–RAGE interaction, downregulation of sRAGE expression, and use of antioxidants. In conclusion, the data suggest that AGE–RAGE stress is involved in the development of CAD in obesity, and the therapeutic interventions to reduce AGE–RAGE would be helpful in preventing, regressing, and slowing the progression of CAD in obesity.

Disclosure

None.




Publication History

Article published online:
12 February 2022

© 2022. International College of Angiology. This article is published by Thieme.

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA

 
  • References

  • 1 James PT. Obesity: the worldwide epidemic. Clin Dermatol 2004; 22 (04) 276-280
  • 2 Eckel RH, York DA, Rössner S. et al; American Heart Association. Prevention Conference VII: Obesity, a worldwide epidemic related to heart disease and stroke: executive summary. Circulation 2004; 110 (18) 2968-2975
  • 3 World Health Organization. Obesity and overweight fact sheet. WHO Media Center. 2016 . Accessed March 27, 2019: https://www.who.int/newsroom/fact-sheets/detail/obesity-and-overweight
  • 4 Berghöfer A, Pischon T, Reinhold T, Apovian CM, Sharma AM, Willich SN. Obesity prevalence from a European perspective: a systematic review. BMC Public Health 2008; 8: 200
  • 5 Berenson GS, Srinivasan SR, Bao W, Newman III WP, Tracy RE, Wattigney WA. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. N Engl J Med 1998; 338 (23) 1650-1656
  • 6 Wilson PW, D'Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med 2002; 162 (16) 1867-1872
  • 7 Poirier P, Eckel RH. Obesity and cardiovascular disease. Curr Atheroscler Rep 2002; 4 (06) 448-453
  • 8 Poirier P, Giles TD, Bray GA. et al; American Heart Association, Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Circulation 2006; 113 (06) 898-918
  • 9 Eilat-Adar S, Eldar M, Goldbourt U. Association of intentional changes in body weight with coronary heart disease event rates in overweight subjects who have an additional coronary risk factor. Am J Epidemiol 2005; 161 (04) 352-358
  • 10 Sierra-Johnson J, Wright SR, Lopez-Jimenez F, Allison TG. Relation of body mass index to fatal and nonfatal cardiovascular events after cardiac rehabilitation. Am J Cardiol 2005; 96 (02) 211-214
  • 11 Ades PA, Savage PD. Obesity in coronary heart disease: an unaddressed behavioral risk factor. Prev Med 2017; 104: 117-119
  • 12 Minutello RM, Chou ET, Hong MK. et al. Impact of body mass index on in-hospital outcomes following percutaneous coronary intervention (report from the New York State Angioplasty Registry). Am J Cardiol 2004; 93 (10) 1229-1232
  • 13 Lovren F, Teoh H, Verma S. Obesity and atherosclerosis: mechanistic insights. Can J Cardiol 2015; 31 (02) 177-183
  • 14 Lüscher TF. Atherosclerosis and CAD. Eur Heart J 2015; 36 (08) 457-459
  • 15 Prasad K. AGE-RAGE stress and coronary artery disease. Int J Angiol 2021; 30 (01) 4-14
  • 16 McNair ED, Wells CR, Qureshi AM. et al. Low levels of soluble receptor for advanced glycation end products in non-ST elevation myocardial infarction patients. Int J Angiol 2009; 18 (04) 187-192
  • 17 McNair ED, Wells CR, Mabood Qureshi A. et al. Soluble receptors for advanced glycation end products (sRAGE) as a predictor of restenosis following percutaneous coronary intervention. Clin Cardiol 2010; 33 (11) 678-685
  • 18 Caspar-Bell G, Dhar I, Prasad K. Advanced glycation end products (AGEs) and its receptors in the pathogenesis of hyperthyroidism. Mol Cell Biochem 2016; 414 (1–2): 171-178
  • 19 Prasad K, Mishra M. Do advanced glycation end products and its receptor play a role in pathophysiology of hypertension?. Int J Angiol 2017; 26 (01) 1-11
  • 20 Zhou Z, Wang K, Penn MS. et al. Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury. Circulation 2003; 107 (17) 2238-2243
  • 21 Sakaguchi T, Yan SF, Yan SD. et al. Central role of RAGE-dependent neointimal expansion in arterial restenosis. J Clin Invest 2003; 111 (07) 959-972
  • 22 Prasad K. Soluble receptor for advanced glycation end products (sRAGE) and cardiovascular disease. Int J Angiol 2006; 15: 57-68
  • 23 Bucala R, Cerami A. Advanced glycosylation: chemistry, biology, and implications for diabetes and aging. Adv Pharmacol 1992; 23: 1-34
  • 24 Tam XHL, Shiu SWM, Leng L, Bucala R, Betteridge DJ, Tan KC. Enhanced expression of receptor for advanced glycation end-products is associated with low circulating soluble isoforms of the receptor in Type 2 diabetes. Clin Sci (Lond) 2011; 120 (02) 81-89
  • 25 Zhang L, Bukulin M, Kojro E. et al. Receptor for advanced glycation end products is subjected to protein ectodomain shedding by metalloproteinases. J Biol Chem 2008; 283 (51) 35507-35516
  • 26 Miyoshi A, Koyama S, Sasagawa-Monden M. et al. JNK and ATF4 as two important platforms for tumor necrosis factor-α-stimulated shedding of receptor for advanced glycation end products. FASEB J 2019; 33 (03) 3575-3589
  • 27 Yonekura H, Yamamoto Y, Sakurai S. et al. Novel splice variants of the receptor for advanced glycation end-products expressed in human vascular endothelial cells and pericytes, and their putative roles in diabetes-induced vascular injury. Biochem J 2003; 370 (Pt 3): 1097-1109
  • 28 Prasad K, Dhar I, Zhou Q, Elmoselhi H, Shoker M, Shoker A. AGEs/sRAGE, a novel risk factor in the pathogenesis of end-stage renal disease. Mol Cell Biochem 2016; 423 (1–2): 105-114
  • 29 Koyama H, Shoji T, Yokoyama H. et al. Plasma level of endogenous secretory RAGE is associated with components of the metabolic syndrome and atherosclerosis. Arterioscler Thromb Vasc Biol 2005; 25 (12) 2587-2593
  • 30 Bucala R, Makita Z, Vega G. et al. Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. Proc Natl Acad Sci U S A 1994; 91 (20) 9441-9445
  • 31 Brownlee M, Vlassara H, Cerami A. Nonenzymatic glycosylation products on collagen covalently trap low-density lipoprotein. Diabetes 1985; 34 (09) 938-941
  • 32 Bucala R, Makita Z, Koschinsky T, Cerami A, Vlassara H. Lipid advanced glycosylation: pathway for lipid oxidation in vivo. Proc Natl Acad Sci U S A 1993; 90 (14) 6434-6438
  • 33 Horiuchi S, Sakamoto Y, Sakai M. Scavenger receptors for oxidized and glycated proteins. Amino Acids 2003; 25 (3–4): 283-292
  • 34 Haberland ME, Fless GM, Scanu AM, Fogelman AM. Malondialdehyde modification of lipoprotein(a) produces avid uptake by human monocyte-macrophages. J Biol Chem 1992; 267 (06) 4143-4151
  • 35 Makita T, Tanaka A, Numano F. Effect of glycated low density lipoprotein on smooth muscle cell proliferation. Int Angiol 1999; 18 (04) 331-334
  • 36 Kamtchueng Simo O, Ikhlef S, Berrougui H, Khalil A. Advanced glycation end products affect cholesterol homeostasis by impairing ABCA1 expression on macrophages. Can J Physiol Pharmacol 2017; 95 (08) 977-984
  • 37 Brown BE, Dean RT, Davies MJ. Glycation of low-density lipoproteins by methylglyoxal and glycolaldehyde gives rise to the in vitro formation of lipid-laden cells. Diabetologia 2005; 48 (02) 361-369
  • 38 Sims TJ, Rasmussen LM, Oxlund H, Bailey AJ. The role of glycation cross-links in diabetic vascular stiffening. Diabetologia 1996; 39 (08) 946-951
  • 39 Chang JB, Chu NF, Syu JT, Hsieh AT, Hung YR. Advanced glycation end products (AGEs) in relation to atherosclerotic lipid profiles in middle-aged and elderly diabetic patients. Lipids Health Dis 2011; 10: 228
  • 40 Brownlee M, Cerami A, Vlassara H. Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications. N Engl J Med 1988; 318 (20) 1315-1321
  • 41 Quehenberger P, Bierhaus A, Fasching P. et al. Endothelin 1 transcription is controlled by nuclear factor-kappaB in AGE-stimulated cultured endothelial cells. Diabetes 2000; 49 (09) 1561-1570
  • 42 Sutton G, Pugh D, Dhaun N. Developments in the role of endothelin-1 in atherosclerosis: a potential therapeutic target?. Am J Hypertens 2019; 32 (09) 813-815
  • 43 Bucala R, Tracey KJ, Cerami A. Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes. J Clin Invest 1991; 87 (02) 432-438
  • 44 Xu B, Chibber R, Ruggiero D, Kohner E, Ritter J, Ferro A. Impairment of vascular endothelial nitric oxide synthase activity by advanced glycation end products. FASEB J 2003; 17 (10) 1289-1291
  • 45 Rojas A, Romay S, González D, Herrera B, Delgado R, Otero K. Regulation of endothelial nitric oxide synthase expression by albumin-derived advanced glycosylation end products. Circ Res 2000; 86 (03) E50-E54
  • 46 Goldin A, Beckman JA, Schmidt AM, Creager MA. Advanced glycation end products: sparking the development of diabetic vascular injury. Circulation 2006; 114 (06) 597-605
  • 47 Hogan M, Cerami A, Bucala R. Advanced glycosylation endproducts block the antiproliferative effect of nitric oxide. Role in the vascular and renal complications of diabetes mellitus. J Clin Invest 1992; 90 (03) 1110-1115
  • 48 Wautier MP, Chappey O, Corda S, Stern DM, Schmidt AM, Wautier JL. Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE. Am J Physiol Endocrinol Metab 2001; 280 (05) E685-E694
  • 49 Schreck R, Rieber P, Baeuerle PA. Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1. EMBO J 1991; 10 (08) 2247-2258
  • 50 Reznikov LL, Waksman J, Azam T. et al. Effect of advanced glycation end products on endotoxin-induced TNF-alpha, IL-1beta and IL-8 in human peripheral blood mononuclear cells. Clin Nephrol 2004; 61 (05) 324-336
  • 51 Stassen M, Müller C, Arnold M. et al. IL-9 and IL-13 production by activated mast cells is strongly enhanced in the presence of lipopolysaccharide: NF-kappa B is decisively involved in the expression of IL-9. J Immunol 2001; 166 (07) 4391-4398
  • 52 Basta G, Lazzerini G, Massaro M. et al. Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses. Circulation 2002; 105 (07) 816-822
  • 53 Chiu JJ, Wung BS, Shyy JY, Hsieh HJ, Wang DL. Reactive oxygen species are involved in shear stress-induced intercellular adhesion molecule-1 expression in endothelial cells. Arterioscler Thromb Vasc Biol 1997; 17 (12) 3570-3577
  • 54 Fraticelli A, Serrano Jr CV, Bochner BS, Capogrossi MC, Zweier JL. Hydrogen peroxide and superoxide modulate leukocyte adhesion molecule expression and leukocyte endothelial adhesion. Biochim Biophys Acta 1996; 1310 (03) 251-259
  • 55 Willam C, Schindler R, Frei U, Eckardt KU. Increases in oxygen tension stimulate expression of ICAM-1 and VCAM-1 on human endothelial cells. Am J Physiol 1999; 276 (06) H2044-H2052
  • 56 Matsui T, Yamagishi S, Ueda S. et al. Telmisartan, an angiotensin II type 1 receptor blocker, inhibits advanced glycation end-product (AGE)-induced monocyte chemoattractant protein-1 expression in mesangial cells through downregulation of receptor for AGEs via peroxisome proliferator-activated receptor-gamma activation. J Int Med Res 2007; 35 (04) 482-489
  • 57 Yamagishi S, Inagaki Y, Okamoto T. et al. Advanced glycation end product-induced apoptosis and overexpression of vascular endothelial growth factor and monocyte chemoattractant protein-1 in human-cultured mesangial cells. J Biol Chem 2002; 277 (23) 20309-20315
  • 58 Sasaki T, Horiuchi S, Yamazaki M, Yui S. Induction of GM-CSF production of macrophages by advanced glycation end products of the Maillard reaction. Biosci Biotechnol Biochem 1999; 63 (11) 2011-2013
  • 59 Kirstein M, Aston C, Hintz R, Vlassara H. Receptor-specific induction of insulin-like growth factor I in human monocytes by advanced glycosylation end product-modified proteins. J Clin Invest 1992; 90 (02) 439-446
  • 60 Kirstein M, Brett J, Radoff S, Ogawa S, Stern D, Vlassara H. Advanced protein glycosylation induces transendothelial human monocyte chemotaxis and secretion of platelet-derived growth factor: role in vascular disease of diabetes and aging. Proc Natl Acad Sci U S A 1990; 87 (22) 9010-9014
  • 61 Wolf YG, Rasmussen LM, Ruoslahti E. Antibodies against transforming growth factor-β 1 suppress intimal hyperplasia in a rat model. J Clin Invest 1994; 93 (03) 1172-1178
  • 62 Sakata N, Meng J, Takebayashi S. Effects of advanced glycation end products on the proliferation and fibronectin production of smooth muscle cells. J Atheroscler Thromb 2000; 7 (03) 169-176
  • 63 Higashi T, Sano H, Saishoji T. et al. The receptor for advanced glycation end products mediates the chemotaxis of rabbit smooth muscle cells. Diabetes 1997; 46 (03) 463-472
  • 64 Prasad K, Tiwari S. Therapeutic interventions for advanced glycation-end products and its receptor- mediated cardiovasculardisease. Curr Pharm Des 2017; 23 (06) 937-943
  • 65 Maillard-Lefebvre H, Boulanger E, Daroux M, Gaxatte C, Hudson BI, Lambert M. Soluble receptor for advanced glycation end products: a new biomarker in diagnosis and prognosis of chronic inflammatory diseases. Rheumatology (Oxford) 2009; 48 (10) 1190-1196
  • 66 Lue LF, Walker DG, Jacobson S, Sabbagh M. Receptor for advanced glycation end products: its role in Alzheimer's disease and other neurological diseases. Future Neurol 2009; 4 (02) 167-177
  • 67 Wendt T, Harja E, Bucciarelli L. et al. RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes. Atherosclerosis 2006; 185 (01) 70-77
  • 68 Prasad K, Mishra M. AGE-RAGE stress, stressors, and antistressors in health and disease. Int J Angiol 2018; 27 (01) 1-12
  • 69 Uribarri J, Cai W, Woodward M. et al. Elevated serum advanced glycation endproducts in obese indicate risk for the metabolic syndrome: a link between healthy and unhealthy obesity?. J Clin Endocrinol Metab 2015; 100 (05) 1957-1966
  • 70 Amin MN, Mosa AA, El-Shishtawy MM. Clinical study of advanced glycation end products in egyptian diabetic obese and non-obese patients. Int J Biomed Sci 2011; 7 (03) 191-200
  • 71 Sebeková K, Somoza V, Jarcusková M, Heidland A, Podracká L. Plasma advanced glycation end products are decreased in obese children compared with lean controls. Int J Pediatr Obes 2009; 4 (02) 112-118
  • 72 Accacha S, Rosenfeld W, Jacobson A. et al. Plasma advanced glycation end products (AGEs), receptors for AGEs and their correlation with inflammatory markers in middle school-age children. Horm Res Paediatr 2013; 80 (05) 318-327
  • 73 Gaens KHJ, Stehouwer CDA, Schalkwijk CG. Advanced glycation endproducts and its receptor for advanced glycation endproducts in obesity. Curr Opin Lipidol 2013; 24 (01) 4-11
  • 74 Foroumandi E, Alizadeh M, Kheirouri S, Asghari Jafarabadi M. Exploring the role of body mass index in relationship of serum nitric oxide and advanced glycation end products in apparently healthy subjects. PLoS One 2019; 14 (03) e0213307
  • 75 Kilhovd BK, Juutilainen A, Lehto S. et al. High serum levels of advanced glycation end products predict increased coronary heart disease mortality in nondiabetic women but not in nondiabetic men: a population-based 18-year follow-up study. Arterioscler Thromb Vasc Biol 2005; 25 (04) 815-820
  • 76 Rodríguez-Mortera R, Luevano-Contreras C, Solorio-Meza S. et al. Soluble Receptor for Advanced Glycation End Products and its correlation with vascular damage in adolescents with obesity. Horm Res Paediatr 2019; 92 (01) 28-35
  • 77 Gaens KHJ, Goossens GH, Niessen PM. et al. Nε-(carboxymethyl)lysine-receptor for advanced glycation end product axis is a key modulator of obesity-induced dysregulation of adipokine expression and insulin resistance. Arterioscler Thromb Vasc Biol 2014; 34 (06) 1199-1208
  • 78 Song F, Hurtado del Pozo C, Rosario R. et al. RAGE regulates the metabolic and inflammatory response to high-fat feeding in mice. Diabetes 2014; 63 (06) 1948-1965
  • 79 Gaens KH, Niessen PM, Rensen SS. et al. Endogenous formation of Nε-(carboxymethyl)lysine is increased in fatty livers and induces inflammatory markers in an in vitro model of hepatic steatosis. J Hepatol 2012; 56 (03) 647-655
  • 80 Jia X, Wu L. Accumulation of endogenous methylglyoxal impaired insulin signaling in adipose tissue of fructose-fed rats. Mol Cell Biochem 2007; 306 (1–2): 133-139
  • 81 Semba RD, Arab L, Sun K, Nicklett EJ, Ferrucci L. Fat mass is inversely associated with serum carboxymethyl-lysine, an advanced glycation end product, in adults. J Nutr 2011; 141 (09) 1726-1730
  • 82 Schmitt A, Gasic-Milenkovic J, Schmitt J. Characterization of advanced glycation end products: mass changes in correlation to side chain modifications. Anal Biochem 2005; 346 (01) 101-106
  • 83 Garay-Sevilla ME, Torres-Graciano S, Villegas-Rodríguez ME, Rivera-Cisneros AE, Wrobel K, Uribarri J. Advanced glycation end products and their receptors did not show any association with body mass parameters in metabolically healthy adolescents. Acta Paediatr 2018; 107 (12) 2146-2151
  • 84 Gugliucci A, Kotani K, Taing J. et al. Short-term low calorie diet intervention reduces serum advanced glycation end products in healthy overweight or obese adults. Ann Nutr Metab 2009; 54 (03) 197-201
  • 85 Ueno H, Koyama H, Shoji T. et al. Receptor for advanced glycation end-products (RAGE) regulation of adiposity and adiponectin is associated with atherogenesis in apoE-deficient mouse. Atherosclerosis 2010; 211 (02) 431-436
  • 86 Leuner B, Max M, Thamm K. et al. RAGE influences obesity in mice. Effects of the presence of RAGE on weight gain, AGE accumulation, and insulin levels in mice on a high fat diet. Z Gerontol Geriatr 2012; 45 (02) 102-108
  • 87 Chiavaroli V, D'Adamo E, Giannini C. et al. Serum levels of receptors for advanced glycation end products in normal-weight and obese children born small and large for gestational age. Diabetes Care 2012; 35 (06) 1361-1363
  • 88 de Giorgis T, D'Adamo E, Giannini C. et al. Could receptors for advanced glycation end products be considered cardiovascular risk markers in obese children?. Antioxid Redox Signal 2012; 17 (02) 187-191
  • 89 D'Adamo E, Giannini C, Chiavaroli V. et al. What is the significance of soluble and endogenous secretory receptor for advanced glycation end products in liver steatosis in obese prepubertal children?. Antioxid Redox Signal 2011; 14 (06) 1167-1172
  • 90 He CT, Lee CH, Hsieh CH. et al. Soluble form of receptor for advanced glycation end products is associated with obesity and metabolic syndrome in adolescents. Int J Endocrinol 2014; 2014: 657607
  • 91 Rowisha M, El-Batch M, El Shikh T, El Melegy S, Aly H. Soluble receptor and gene polymorphism for AGE: relationship with obesity and cardiovascular risks. Pediatr Res 2016; 80 (01) 67-71
  • 92 Miranda ER, Somal VS, Mey JT. et al. Circulating soluble RAGE isoforms are attenuated in obese, impaired-glucose-tolerant individuals and are associated with the development of type 2 diabetes. Am J Physiol Endocrinol Metab 2017; 313 (06) E631-E640
  • 93 Davis KE, Prasad C, Vijayagopal P, Juma S, Imrhan V. Serum soluble receptor for advanced glycation end products correlates inversely with measures of adiposity in young adults. Nutr Res 2014; 34 (06) 478-485
  • 94 Norata GD, Garlaschelli K, Grigore L. et al. Circulating soluble receptor for advanced glycation end products is inversely associated with body mass index and waist/hip ratio in the general population. Nutr Metab Cardiovasc Dis 2009; 19 (02) 129-134
  • 95 Hagen I, Schulte DM, Müller N. et al. Soluble receptor for advanced glycation end products as a potential biomarker to predict weight loss and improvement of insulin sensitivity by a very low calorie diet of obese human subjects. Cytokine 2015; 73 (02) 265-269
  • 96 Guclu M, Ali A, Eroglu DU, Büyükuysal SO, Cander S, Ocak N. Serum levels of sRAGE are associated with body measurements, but not glycemic parameters in patients with prediabetes. Metab Syndr Relat Disord 2016; 14 (01) 33-39
  • 97 Dozio E, Briganti S, Delnevo A. et al. Relationship between soluble receptor for advanced glycation end products (sRAGE), body composition and fat distribution in healthy women. Eur J Nutr 2017; 56 (08) 2557-2564
  • 98 Brix JM, Höllerl F, Kopp HP, Schernthaner GH, Schernthaner G. The soluble form of the receptor of advanced glycation endproducts increases after bariatric surgery in morbid obesity. Int J Obes 2012; 36 (11) 1412-1417
  • 99 Miranda ER, Fuller KNZ, Perkins RK. et al. Endogenous secretory RAGE increases with improvements in body composition and is associated with markers of adipocyte health. Nutr Metab Cardiovasc Dis 2018; 28 (11) 1155-1165
  • 100 Vazzana N, Guagnano MT, Cuccurullo C. et al. Endogenous secretory RAGE in obese women: association with platelet activation and oxidative stress. J Clin Endocrinol Metab 2012; 97 (09) E1726-E1730
  • 101 Prasad K. Is there any evidence that AGE/sRAGE is a universal biomarker/risk marker for diseases?. Mol Cell Biochem 2019; 451 (1-2): 139-144
  • 102 Prasad K. Pathophysiology of atherosclerosis. In: Chang JB, Olsen ER, Prasad K, Sumpio BE. eds. Textbook of Angiology. New York, NY: Springer-Verlag; 2000: 85-105
  • 103 Prasad K, Bhanumathy KK. AGE-RAGE axis in the pathophysiology of chronic lower limb ischemia and a novel strategy for its treatment. Int J Angiol 2020; 29 (03) 156-167
  • 104 Nowak WN, Deng J, Ruan XZ, Xu Q. Reactive oxygen species generation and atherosclerosis. Arterioscler Thromb Vasc Biol 2017; 37 (05) e41-e52
  • 105 Kattoor AJ, Pothineni NVK, Palagiri D, Mehta JL. Oxidative stress in atherosclerosis. Curr Atheroscler Rep 2017; 19 (11) 42
  • 106 Makki K, Froguel P, Wolowczuk I. Adipose tissue in obesity-related inflammation and insulin resistance: cells, cytokines, and chemokines. ISRN Inflamm 2013; 2013: 139239
  • 107 Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease. Circ Res 2005; 96 (09) 939-949
  • 108 Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA 1999; 282 (22) 2131-2135
  • 109 Prasad K. C-reactive protein and cardiovascular diseases. Int J Angiol 2003; 12: 1-12
  • 110 Prasad K. C-reactive protein increases oxygen radical generation by neutrophils. J Cardiovasc Pharmacol Therapeut 2004; 9 (03) 203-209