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Oxidative Stress and Vascular Disease
Abstract
Growing evidence indicates that chronic and acute overproduction of reactive oxygen species (ROS) under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). These ROS can be released from nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, lipoxygenase, mitochondria, or the uncoupling of nitric oxide synthase in vascular cells. ROS mediate various signaling pathways that underlie vascular inflammation in atherogenesis: from the initiation of fatty streak development through lesion progress to ultimate plaque rupture. Various animal models of oxidative stress support the notion that ROS have a causal role in atherosclerosis and other cardiovascular diseases. Human investigations also support the oxidative stress hypothesis of atherosclerosis. Oxidative stress is the unifying mechanism for many CVD risk factors, which additionally supports its central role in CVD. Despite the demonstrated role of antioxidants in cellular and animal studies, the ineffectiveness of antioxidants in reducing cardiovascular death and morbidity in clinical trials has led many investigators to question the importance of oxidative stress in human atherosclerosis. Others have argued that the prime factor for the mixed outcomes from using antioxidants to prevent CVD may be the lack of specific and sensitive biomarkers by which to assess the oxidative stress phenotypes underlying CVD. A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular locales, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research in this area as we move toward the broader use of pharmacological and regenerative therapies in the treatment and prevention of CVD.
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“Additionally, studies show peroxynitrite can traverse cell membranes by both diffusion and through ion channels, suggesting that peroxynitrite can mediate oxidation/nitration distant from its site of formation (221, 611).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [611]
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“Additionally, studies show peroxynitrite can traverse cell membranes by both diffusion and through ion channels, suggesting that peroxynitrite can mediate oxidation/nitration distant from its site of formation (221, 611).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [611]
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Citations
Cites
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., Izzo, J. L., Jones, D. W., Materson, B. J., Oparil, S., Wright, J. T., et al. (2003) · Hypertension · doi:10.1161/01.hyp.0000107251.49515.c2 · Cited by 13,271
The pathogenesis of atherosclerosis: a perspective for the 1990s
Ross, R. (1993) · Nature · doi:10.1038/362801a0 · Cited by 10,618
Free Radicals in the Physiological Control of Cell Function
Dröge, W. (2002) · Physiological Reviews · doi:10.1152/physrev.00018.2001 · Cited by 9,855
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
Role of Oxidative Stress in Development of Complications in Diabetes
Baynes, J. (1991) · Diabetes · doi:10.2337/diab.40.4.405 · Cited by 3,791
Fridovich (1978) · doi:10.1126/science.210504 · Cited by 3,329
Mitochondrial diseases in man and mouse
Wallace, D. C. (1999) · Science · doi:10.1126/science.283.5407.1482 · Cited by 3,060
NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
Griendling, K. K., Sorescu, D., & Ushio-Fukai, M. (2000) · Circulation Research · doi:10.1161/01.res.86.5.494 · Cited by 2,886
Requirement for Generation of H 2 O 2 for Platelet-Derived Growth Factor Signal Transduction
Sundaresan, M., Yu, Z.-X., Ferrans, V. J., Irani, K., & Finkel, T. (1995) · Science · doi:10.1126/science.270.5234.296 · Cited by 2,520
Research works printed but not linked: 33
- 10.1093/ije/18.3_Supplement_1.S20 · DOI
- 10.1161/atvb.16.7.831 · DOI
- 10.1161/res.80.6.810 · DOI
- 1996, Am J Physiol, 271, H1626
- 10.1161/res.86.5.494 · DOI
- 10.1161/circ.99.15.2027 · DOI
- 10.1161/atvb.21.5.739 · DOI
- 10.1161/atvb.22.1.21 · DOI
- 10.1161/circ.101.12.1372 · DOI
- 10.1161/circ.103.10.1446 · DOI
- 10.1161/circ.103.9.1282 · DOI
- 10.1161/res.86.9.960 · DOI
- 10.1161/hyp.38.6.1395 · DOI
- 10.1161/circ.105.3.393 · DOI
- 10.1161/hyp.37.6.1450 · DOI
- 10.1161/res.89.5.408 · DOI
- 10.1161/hyp.37.2.334 · DOI
- 10.1161/circ.101.14.1653 · DOI
- 10.1161/circ.98.8.794 · DOI
- 10.1161/hyp.32.3.488 · DOI
- 10.1161/res.85.5.437 · DOI
- 10.1161/res.85.4.357 · DOI
- 1994, Am J Physiol, 267, H1804
- 10.1161/res.87.3.241 · DOI
- 10.1161/str.31.8.1889 · DOI
- 10.1161/circ.99.2.224 · DOI
- 10.1161/circ.103.12.1618 · DOI
- 10.1161/res.88.2.e14 · DOI
- 10.1161/circ.101.11.1261 · DOI
- 10.1161/atvb.21.9.1451 · DOI
- 10.1161/circ.88.4.8403327 · DOI
- 10.1161/circ.105.7.849 · DOI
- 10.1161/res.87.12.1074 · DOI
Cited by
Sorted by citations
Role of Oxidative Modifications in Atherosclerosis
Stocker, R., & Keaney, J. F. (2004) · Physiological Reviews · doi:10.1152/physrev.00047.2003 · Cited by 2,651
The clinical implications of endothelial dysfunction
Widlansky, M. E., Gokce, N., Keaney, J. F., & Vita, J. A. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(03)00994-x · Cited by 1,749
Role of oxidative stress in female reproduction
Agarwal, A., Gupta, S., & Sharma, R. K. (2005) · Reproductive Biology and Endocrinology · doi:10.1186/1477-7827-3-28 · Cited by 1,729
Jones, D. P. (2006) · Antioxidants & Redox Signaling · doi:10.1089/ars.2006.8.1865 · Cited by 1,726
“titative measures of disease outcome (11, 14, 19, 41, 42, 49 55, 62, 67).”
Aryal, S., Baniya, M. K., Danekhu, K., Kunwar, P., Gurung, R., & Koirala, N. (2019) · Plants · doi:10.3390/plants8040096 · Cited by 1,365
“The generation of highly reactive oxygen species (ROS) with a lone unpaired electron induce oxidative stress and plays a key role in the pathogenesis of numerous physiological conditions, including cellular injury, aging, cancer, and hepatic, neurodegenerative, cardiovascular and renal disorders [1,2].”
BackgroundSmoking and Cardiovascular Disease
Meßner, B., & Bernhard, D. (2014) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.113.300156 · Cited by 1,215
Kregel, K. C., & Zhang, H. J. (2007) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00327.2006 · Cited by 883
“Interestingly, a common phenomenon in agingrelated pathologies is the discovery of ROS as a potential unifying mechanism contributing to many of these diseases (72, 150, 176, 205).”
BackgroundRole of ROS and Nutritional Antioxidants in Human Diseases
Liu, Z., Ren, Z., Zhang, J., Chuang, C.-C., Kandaswamy, E., Zhou, T., & Zuo, L. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00477 · Cited by 860
“SMCs can secret extracellular matrix that forms a thin fibrous cap surrounding the fatty streak (Madamanchi et al., 2005; Cachofeiro et al., 2008).”
BackgroundInfluentialKontush, A., & Chapman, M. J. (2006) · Pharmacological Reviews · doi:10.1124/pr.58.3.1 · Cited by 647
“Various oxidative systems potentially contribute to LDL oxidation in vivo, and these include NAD(P)H oxidases, xanthine oxidase, myeloperoxidase, uncoupled nitric oxide synthase (NOS), lipoxygenases, and the mitochondrial electron transport chain (Madamanchi et al., 2005; Mueller et al., 2005).”
BackgroundGambini, J., Inglés, M., González, G. O., López-Grueso, R., Bonet-Costa, V., Gimeno-Mallench, L., Mas‐Bargues, C., Abdelaziz, K. M., Gómez‐Cabrera, M. C., Viña, J., et al. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2015/837042 · Cited by 779
“Oxidative damage is involved in the pathogenesis ofmany important diseases, such as diabetes [66], cardiovascular diseases [67], neurodegenerative diseases [68], and cancer [69].”
BackgroundAbderrazak, A., Syrovets, T., Couchie, D., Hadri, K. E., Friguet, B., Simmet, T., & Rouis, M. (2015) · Redox Biology · doi:10.1016/j.redox.2015.01.008 · Cited by 749
“Immune cells (macrophages and T cells), foam cells, vascular endothelial cells, smooth muscle cells (SMCs), platelets, extracellular matrix and a lipid rich core with extensive necrosis and fibrosis of surrounding tissues constitute the basic elements of atherosclerotic plaques [136,137].”
BackgroundProgress and Challenges in Metabolic Syndrome in Children and Adolescents
Steinberger, J., Daniels, S. R., Eckel, R. H., Hayman, L. L., Lustig, R. H., McCrindle, B. W., & Mietus‐Snyder, M. (2009) · Circulation · doi:10.1161/circulationaha.108.191394 · Cited by 721
Tu, W., Wang, H., Li, S., Liu, Q., & Sha, H. (2018) · Aging and Disease · doi:10.14336/ad.2018.0513 · Cited by 727
“ROS contribute to endothelial dysfunction and subsequent formation of atherosclerotic lesions [9].”
BackgroundVascular complications in diabetes mellitus: the role of endothelial dysfunction
Schalkwijk, C. G., & Stehouwer, C. D. A. (2005) · Clinical Science · doi:10.1042/cs20050025 · Cited by 670
The Potential Benefits of Red Beetroot Supplementation in Health and Disease
Clifford, T., Howatson, G., West, D., & Stevenson, E. (2015) · Nutrients · doi:10.3390/nu7042801 · Cited by 635
“This imbalance may overwhelm the endogenous antioxidant defence network leaving DNA, carbohydrate, protein and lipid structures susceptible to oxidation and functional impairments [45–47].”
BackgroundReactive Oxygen Species Activate the HIF-1α Promoter Via a Functional NFκB Site
Bonello, S., Zähringer, C., BelAiba, R. S., Djordjevic, T., Hess, J., Michiels, C., Kietzmann, T., & Görlach, A. (2007) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000258979.92828.bc · Cited by 626
Vascular Actions of Estrogens: Functional Implications
Miller, V. M., & DUCKLES, S. P. (2008) · Pharmacological Reviews · doi:10.1124/pr.107.08002 · Cited by 608
Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis
Kaneto, H., Katakami, N., Matsuhisa, M., & Matsuoka, T. (2010) · Mediators of Inflammation · doi:10.1155/2010/453892 · Cited by 590
“It has been suggested that ROS regulate expression of various growth factors and several growthrelated protooncogenes such as c-Myc, c-Fos and c-Jun [124, 125].”
BackgroundKell, D. B. (2009) · BMC Medical Genomics · doi:10.1186/1755-8794-2-2 · Cited by 554
“Atherosclerosis is a progressive inflammatory disease [637-667] characterized by the accumulation of both oxidised lipids and various fibrous elements in arteries, often as plaques [668; 669].”
BackgroundDirect Evidence of Endothelial Oxidative Stress With Aging in Humans
Donato, A. J., Eskurza, I., Silver, A., Levy, A., Pierce, G. L., Gates, P. E., & Seals, D. R. (2007) · Circulation Research · doi:10.1161/01.res.0000269183.13937.e8 · Cited by 566
Francque, S., van der Graaff, D., & Kwanten, W. J. (2016) · Journal of Hepatology · doi:10.1016/j.jhep.2016.04.005 · Cited by 591
“Increased oxidative stress [71,72] Oxidative stress, plays a central role in pathophysiology of CVD [73]”
BackgroundPositive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species
Bashan, N., Kovsan, J., Kachko, I., Ovadia, H., & Rudich, A. (2009) · Physiological Reviews · doi:10.1152/physrev.00014.2008 · Cited by 542
“transformation (405), atherosclerosis (268, 403), neurode-”
Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation
Tejero, J., Shiva, S., & Gladwin, M. T. (2019) · Physiological Reviews · doi:10.1152/physrev.00036.2017 · Cited by 541
Hordijk, P. L. (2006) · Circulation Research · doi:10.1161/01.res.0000204727.46710.5e · Cited by 534
Phagocytosis of apoptotic cells by macrophages is impaired in atherosclerosis
Schrijvers, D. M., De Meyer, G. R. Y., Kockx, M. M., Herman, A. G., & Martinet, W. (2005) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000166517.18801.a7 · Cited by 509
Oxidative stress and atherosclerosis
Singh, U. S., & Jialal, I. (2006) · Pathophysiology · doi:10.1016/j.pathophys.2006.05.002 · Cited by 497
“[4] N.”
BackgroundProtective effects of sirtuins in cardiovascular diseases: from bench to bedside
Winnik, S., Auwerx, J., Sinclair, D. A., & Matter, C. M. (2015) · European Heart Journal · doi:10.1093/eurheartj/ehv290 · Cited by 422
“DNA damage, and progressive respiratory chain dysfunction activate several signalling pathways underlying endothelial dysfunction and vascular inflammation in atherogenesis.(33) Sirt3-dependent transcriptional induction of SOD2 and catalase was shown to prevent”
BackgroundEndothelial dysfunction : the early predictor of atherosclerosis
Mudau, M., Genis, A., Lochner, A., & Strijdom, H. (2012) · Cardiovascular Journal of Africa · doi:10.5830/cvja-2011-068 · Cited by 521
Cardiovascular Effects of Pulmonary Exposure to Single-Wall Carbon Nanotubes
Li, Z., Hulderman, T., Salmen, R., Chapman, R. S., Leonard, S. S., Young, S., Shvedova, A. A., Luster, M. I., & Simeonova, P. P. (2006) · Environmental Health Perspectives · doi:10.1289/ehp.9688 · Cited by 413
“Environmental Health Perspectives • VOLUME 115 | NUMBER 3 | March 2007 381 environmental insults (Madamanchi et al. 2005), and mitochondrial dysfunction is emerging as an important pathophysiologic factor in a number of cardiovascular diseases including atherosclerosis (Binkova et al.”
BackgroundDiabetic Cardiovascular Disease Induced by Oxidative Stress
Kayama, Y., Raaz, U., Jagger, A. L., Adam, M., Schellinger, I. N., Sakamoto, M., Suzuki, H., Toyama, K., Spin, J. M., & Tsao, P. S. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161025234 · Cited by 421
“Interestingly, while LOX metabolites of AA mediate angiotensin II stimulation of NAD(P)H oxidase in VSMC [37], AA metabolism is itself another source of ROS production in vascular cells [38].”
BackgroundOxidative Stress in Diabetes: Implications for Vascular and Other Complications
Pitocco, D., Tesauro, M., Rizzi, A., Ghirlanda, G., & Cardillo, C. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms141121525 · Cited by 413
“The functional effects of RS range from physiology to pathophysiology: vascular tone [33], cell adhesion [34], immune responses [35], cell growth and hormone action [36] are all examples of RS participation in normal physiology; on the other hand, a causative role of RS has been involved in ageing [37], cancer [38], a…”
BackgroundJung, T., Catalgol, B., & Grune, T. (2009) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2009.04.001 · Cited by 401
Endothelial Dysfunction, Inflammation, and Apoptosis in Diabetes Mellitus
van den Oever, I. A., Raterman, H. G., Nurmohamed, M. T., & Şimşek, S. (2010) · Mediators of Inflammation · doi:10.1155/2010/792393 · Cited by 378
“Finally ROS can modify endothelial function by a variety of mechanisms, like peroxidation of membrane lipids, activation of NF-κB, and decreasing the availability of NO [91].”
BackgroundKell, D. B. (2010) · Archives of Toxicology · doi:10.1007/s00204-010-0577-x · Cited by 361
“…et al. 2009; Grainger 2007; Hansson 2001, 2005; Himmelfarb et al. 2002; Kibel et al. 2008; Kunsch and Medford 1999; Libby 2002; Libby et al. 2002; Madamanchi et al. 2005a, b; Mullenix et al. 2005; Nigro et al. 2006; Packard and Libby 2008; Paoletti et al. 2004; Popa et al. 2007; Rader and…”
BackgroundTsimikas, S., Bergmark, C., Beyer, R. W., Patel, R., Pattison, J., Miller, E. R., Juliano, J., & Witztum, J. L. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(02)02769-9 · Cited by 348
Oxidative Stress, Nitric Oxide, and Diabetes
Pitocco, D., Zaccardi, F., Stasio, E. D., Romitelli, F., Santini, S. A., Zuppi, C., & Ghirlanda, G. (2010) · The Review of Diabetic Studies · doi:10.1900/rds.2010.7.15 · Cited by 345
“On the other hand, a causative role of RS has been implicated in ageing [36], cancer [37], atherosclerosis [38], neurodegenerative diseases [39], obesity, and diabetes [40].”
BackgroundReview: reactive oxygen and nitrogen species and functional adaptation of the placenta
Myatt, L. (2010) · Placenta · doi:10.1016/j.placenta.2009.12.021 · Cited by 330
“There may be several cellular sources in the placenta including the mitochondrial electron transport chain [21], xanthine oxidase [22] and NADPH oxidase (NOX) [23], Previously Raijmakers et al.”
BackgroundOxidative stress and cardiovascular disease: Novel tools give (free) radical insight
Fearon, I. M., & Faux, S. P. (2009) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2009.05.013 · Cited by 334
Lu, T., & Finkel, T. (2008) · Experimental Cell Research · doi:10.1016/j.yexcr.2008.01.011 · Cited by 327
“A long standing notion is that many if not all of the identified risk factors contribute to vascular disease by inducing redox stress within the vessel wall [29].”
BackgroundFree Radicals, Mitochondria, and Oxidized Lipids
Gutiérrez, J., Ballinger, S. W., Darley-Usmar, V. M., & Landar, A. L. (2006) · Circulation Research · doi:10.1161/01.res.0000248212.86638.e9 · Cited by 320
Type 2 Diabetes Mellitus and Hypertension
Lastra, G., Syed, S., Kurukulasuriya, L. R., Manrique, C., & Sowers, J. R. (2014) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2013.09.005 · Cited by 307
“ROS can be produced in different vascular cell types, including endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through activation of xanthine oxidase (XO), nitric oxide (NO) synthase, the mitochondrial respiratory chain, (30-33).”
Biochemical basis and metabolic interplay of redox regulation
Zhang, L., Wang, X., Cueto, R., Effi, C., Zhang, Y., Tan, H., Qin, X., Ji, Y., Yang, X., & Wang, H. (2019) · Redox Biology · doi:10.1016/j.redox.2019.101284 · Cited by 308
“Besides, Mitochondrial ROS induced by various CVD risk factors are involved in EC activation/dysfunction, SMC proliferation/migration, dendritic cell differentiation, atherosclerosis, and other inflammatory disease [93].”
BackgroundInfluentialTotal Antioxidant Capacity: a biomarker in biomedical and nutritional studies
Kusano, C., & Ferrari, B. (2008) · Journal of cell & molecular biology · Cited by 304
Non-Invasive Vascular Function Tests:
Tomiyama, H., & Yamashina, A. (2009) · Circulation Journal · doi:10.1253/circj.cj-09-0534 · Cited by 298
Roles of Oxidative Stress and Inflammation in Vascular Endothelial Dysfunction-Related Disease
Higashi, Y. (2022) · Antioxidants · doi:10.3390/antiox11101958 · Cited by 326
“NADPH oxidase is a novel enzyme that is involved in the production of ROS in human vascular endothelial cells and VSMCs [48,49].”
BackgroundMartins, A. R., Nachbar, R. T., Gorjão, R., Vinolo, M. A. R., Festuccia, W. T., Lambertucci, R. H., Cury‐Boaventura, M. F., Silveira, L. R., Curi, R., & Hirabara, S. M. (2012) · Lipids in Health and Disease · doi:10.1186/1476-511x-11-30 · Cited by 306
“Conversely, a negative role of ROS has been implicated in ageing-related diseases, malignant transformation, atherosclerosis, neurodegenerative diseases, obesity, and diabetes [88,94,95].”
Zhang, R., Zhao, J., Han, G., Liu, Z., Liu, C., Zhang, C., Liu, B., Jiang, C., Liu, R., Zhao, T., et al. (2016) · Journal of the American Chemical Society · doi:10.1021/jacs.5b12848 · Cited by 287
Yu, E., Calvert, P. A., Mercer, J. R., Harrison, J. B., Baker, L. L., Figg, N. L., Kumar, S., Wang, J. C., Hurst, L. A., Obaid, D. R., et al. (2013) · Circulation · doi:10.1161/circulationaha.113.002271 · Cited by 288
Combating oxidative stress disorders with citrus flavonoid: Naringenin
Zaidun, N. H., Thent, Z. C., & Latiff, A. A. (2018) · Life Sciences · doi:10.1016/j.lfs.2018.07.017 · Cited by 266
Involvement of Oxidative Stress in the Pathogenesis of Diabetes
Kaneto, H., Katakami, N., Kawamori, D., Miyatsuka, T., Sakamoto, K., Matsuoka, T., Matsuhisa, M., & Yamasaki, Y. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2006.1465 · Cited by 267
“Taken together, activation of the JNK pathway triggers VSMC proliferation, leading to neointimal formation, and the JNK pathway could be a new therapeutic target for atherosclerosis (cid:5) (cid:5) Activation of the JNK pathway was closely correlated with the presence of clearly established plaques…”
Plasma membrane integrity: implications for health and disease
Ammendolia, D. A., Bement, W. M., & Brumell, J. H. (2021) · BMC Biology · doi:10.1186/s12915-021-00972-y · Cited by 279
“Chemical AGEs Type 1 and type 2 diabetes [222, 223]”
BackgroundAssociation between adherence to the Mediterranean diet and oxidative stress
Dai, J., Jones, D. P., Goldberg, J., Ziegler, T. R., Bostick, R. M., Wilson, P. W., Manatunga, A. K., Shallenberger, L., Jones, L., & Vaccarino, V. (2008) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.2008.26528 · Cited by 256
“Oxidative stress is a pathophysiological pathway thought to influence all aspects of atherosclerosis development and cardiovascular disease risk (7).”
BackgroundNrf2 Protects Against Maladaptive Cardiac Responses to Hemodynamic Stress
Li, J., Ichikawa, T., Villacorta, L., Janicki, J. S., Brower, G. L., Yamamoto, M. P., & Cui, T. (2009) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.109.189480 · Cited by 254
“20 (6) B C 4 Arterioscler Thromb Vasc Biol September 2009”
Hypoxia-induced signaling in the cardiovascular system: pathogenesis and therapeutic targets
Zhao, Y., Xiong, W., Li, C., Zhao, R., Lu, H., Song, S., Zhou, Y., Hu, Y., Shi, B., & Ge, J. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01652-9 · Cited by 275
“89,102 Acute hypoxia leads to the activation of ECs, liberating in fl ammatory mediators and growth factors, thereby promoting the adhesion of phagocytes (such as neutrophils and macrophages) to the vascular wall.”
BackgroundOxidative Stress Signaling to Chromatin in Health and Disease
Kreuz, S., & Fischle, W. (2016) · Epigenomics · doi:10.2217/epi-2016-0002 · Cited by 265
Transcriptional responses to oxidative stress: Pathological and toxicological implications
Ma, Q. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.11.004 · Cited by 252
Raspberries and Human Health: A Review
Rao, A. V., & Snyder, D. M. (2010) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf903484g · Cited by 258
Vascular Oxidative Stress: Impact and Therapeutic Approaches
Sena, C. M., Leandro, A., Azul, L., Seiça, R. M. F., & Perry, G. L. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.01668 · Cited by 266
“These substances derive from endothelial cells, vasoactive nerves, and perivascular tissue (Giacco and Brownlee, 2010; Majesky, 2015).”
BackgroundRadical medicine: treating ageing to cure disease
Finkel, T. (2005) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1763 · Cited by 234
“Both animal and human observations indicate that these disparate risk factors can all induce a pro-oxidant environment within the vessel wal”
BackgroundImpact of oxidized low density lipoprotein on vascular cells
Galle, J., Hansen‐Hagge, T. E., Wanner, C., & Seibold, S. (2005) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2005.10.005 · Cited by 239
“Atherosclerosis is considered to be a chronic nflammatory disease [1], and growing evidence indicates hat chronic and acute overproduction of ROS under pathohysiological conditions is relevant for the development of ardiovascular diseases (CVD) [17].”
BackgroundS -Nitrosylation: NO-Related Redox Signaling to Protect Against Oxidative Stress
Sun, J., Steenbergen, C., & Murphy, E. (2006) · Antioxidants and Redox Signaling · doi:10.1089/ars.2006.8.1693 · Cited by 240
“Thus, a large transient increase or a moderate sustained increase in ROS is suggested to be detrimental and to contribute to heart dysfunction and myocyte death (47, 77). of cardiac function (7, 22, 47).”
Reactive carbonyls and oxidative stress: Potential for therapeutic intervention
Ellis, E. M. (2007) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2007.03.015 · Cited by 240
“…imbalance can arise, and can potentially lead to damage, in a variety of disease conditions, including cardiovascular disease and atherosclerosis (Madamanchi et al., 2005), hypertension (Touyz, 2004), inflammatory-based diseases such as chronic obstructive pulmonary disease (MacNee, 2005),…”
BackgroundShen, J.-S., Meng, X., Moore, D. F., Quirk, J. M., Shayman, J. A., Schiffmann, R., & Kaneski, C. R. (2008) · Molecular Genetics and Metabolism · doi:10.1016/j.ymgme.2008.06.016 · Cited by 235
“Growing evidence indicate that excessive production of ROS has a causal role in the development of atherosclerosis and other cardiovascular disorders through a number of mechanisms such as oxidation of low-density lipoprotein and modification of endothelial functions and adhesion molecules [21;22].”
Raynes, R., Pomatto, L. C. D., & Davies, K. J. A. (2016) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2016.05.001 · Cited by 234
LI, Y., Cao, Z., & Zhu, H. (2005) · Pharmacological Research · doi:10.1016/j.phrs.2005.08.002 · Cited by 235
Metabolic stress, reactive oxygen species, and arrhythmia
Jeong, E.-M., Liu, M., Sturdy, M., Gao, G., Varghese, S. T., Sovari, A. A., & Dudley, S. C. (2011) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2011.09.018 · Cited by 243
“Cardiac conditions such as hypertension [30], diabetes mellitus [31], coronary artery disease [32, 33], cardiomyopathies, and HF [34, 35] are associated with altered metabolism and arrhythmias.”
BackgroundCyclic Stretch, Reactive Oxygen Species, and Vascular Remodeling
Birukov, K. G. (2009) · Antioxidants and Redox Signaling · doi:10.1089/ars.2008.2390 · Cited by 233
“Expression of one or more of NADPH oxidase subunits is upregulated in HUVEC culture in response to angiotensin II, endothelin-1,oxidizedlowdensitylipoproteins,pulsatileshear stress, and phorbol esters (51, 102).”
Nolin, T. D., McMenamin, M. E., & Himmelfarb, J. (2007) · Journal of Chromatography B · doi:10.1016/j.jchromb.2007.02.024 · Cited by 228
Lin, Y., Liu, X., Cheng, Y., Yang, J., Huo, Y., & Zhang, C. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m806920200 · Cited by 230
Redox signaling in cardiovascular health and disease
Madamanchi, N. R., & Runge, M. S. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.04.001 · Cited by 227
Self-citationROS-Scavenging Therapeutic Hydrogels for Modulation of the Inflammatory Response
Kim, Y. E., & Kim, J. (2021) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.1c18261 · Cited by 235
Manrique, C. M., Lastra, G., Gardner, M., & Sowers, J. R. (2009) · Medical Clinics of North America · doi:10.1016/j.mcna.2009.02.014 · Cited by 232
“availability of 5,6,7,8-tetrahydrobiopterin (a cofactor in NO production) or the substrate L-arginine, eNOS switches from this coupled state to an uncoupled state, in which electrons from the heme group reduce oxygen, resulting in production of O2 .(28) This uncoupling of eNOS appears to play an important role in endo…”
BackgroundInfluentialVendrov, A. E., Vendrov, K. C., Smith, A., Yuan, J., Sumida, A., Robidoux, J., Runge, M. S., & Madamanchi, N. R. (2015) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.6221 · Cited by 224
Self-citationAntioxidant effects and mechanism of silymarin in oxidative stress induced cardiovascular diseases
Taleb, A., Ahmad, K. A., Ihsan, A. U., Qu, J., Lin, N., Hezam, K., Koju, N., Hui, L., & Qi-long, D. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.03.140 · Cited by 222
Hypoxia inducible factor as a therapeutic target for atherosclerosis
Jain, T., Nikolopoulou, E. A., Xu, Q., & Qu, A. (2017) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.09.003 · Cited by 216
“Overproduction of free radicals and ROS lead to a of endothelial cell function (Madamanchi et al., 2005).”
BackgroundOxidative Stress and Vascular Disease
Heistad, D. D. (2006) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000203525.62147.28 · Cited by 210
“diseases; and (4) some very recent studies of oxidative stress”
BackgroundVascular biology of hydrogen sulfide
Kanagy, N. L., Szabó, C., & Papapetropoulos, A. (2017) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00329.2016 · Cited by 209
“Enhanced oxidative stress is a key event for diseases affecting the vessel wall including hypertension, atherosclerosis, and vascular diabetic complications (84, 96, 135).”
BackgroundFlavonoids: Antioxidants Against Atherosclerosis
Grassi, D., Desideri, G., & Ferri, C. (2010) · Nutrients · doi:10.3390/nu2080889 · Cited by 205
“The ability of flavonoids and flavonoid-rich foods and beverages to reduce NO oxidation and increase NO bioavailability appears to contribute significantly to its vascular benefits [1,4-6] and thus, finally, to protect against atherosclerosis [1-4].”
BackgroundInfluentialOxInflammation: From Subclinical Condition to Pathological Biomarker
Valacchi, G., Virgili, F., Cervellati, C., & Pecorelli, A. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00858 · Cited by 212
“Relevant to the concept of OxInflammation as a self-perpetuating vicious cycle of cytotoxic substances coming from different sources, these redox-sensitive transcription factors, along with others involved in vascular remodeling, have been implicated in the regulation of vascular NOX (Madamanchi et al., 2005; Singh an…”
BackgroundInfluentialTeratogenic mechanisms of medical drugs
van Gelder, M. M. H. J., van Rooij, I. A. L. M., Miller, R. K., Zielhuis, G. A., den Berg, L. T. W. D. J.-V., & Roeleveld, N. (2010) · Human Reproduction Update · doi:10.1093/humupd/dmp052 · Cited by 210
“It is well known from adult cases of cardiovascular diseases (Madamanchi et al ., 2005) that ROS are extensively formed during reperfusion of ischemic tissues, while there is considerable evidence that hypoxia followed by reperfusion is teratogenic in animal studies (Wellfelt et al ., 1999).”
Redox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases
Cepas, V., Collino, M., Mayo, J. C., & Sainz, R. M. (2020) · Antioxidants · doi:10.3390/antiox9020142 · Cited by 216
“AGE-a s ciat d oxidative str ss appears as a central element in the path logy of atherosclerosis [137].”
BackgroundThe Role of Nrf2-Mediated Pathway in Cardiac Remodeling and Heart Failure
Zhou, S., Sun, W., Zhang, Z., & Zheng, Y. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/260429 · Cited by 205
“It has been well established that oxidative stress is a major cause of HF [1–8].”
Uric Acid Restores Endothelial Function in Patients With Type 1 Diabetes and Regular Smokers
Waring, W. S., McKnight, J. A., Webb, D. J., & Maxwell, S. R. J. (2006) · Diabetes · doi:10.2337/db06-0283 · Cited by 200
“Increased free radical activity in the bloodstream or arterial intima appears to contribute to endothelial dysfunction (11,12), which can be ameliorated by administration of supplementary natural antioxidants, including ascorbic acid and tocopherol (13–15).”
BackgroundOxidative Stress and Inflammation in Renal and Cardiovascular Complications of Diabetes
Charlton, A., Garzarella, J., Jandeleit-Dahm, K. A. M., & Jha, J. C. (2020) · Biology · doi:10.3390/biology10010018 · Cited by 214
“ROS also mediate various signaling pathways that underlie lesion progression and ultimately plaque rupture [82].”
BackgroundVirgilio, A. L. D., Reigosa, M. A., Arnal, P., & de Mele, M. F. L. (2009) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2009.12.089 · Cited by 203
Endothelial dysfunction in rheumatic autoimmune diseases
Murdaca, G., Colombo, B. M., Cagnati, P., Gulli, R., Spanò, F. M., & Puppo, F. (2012) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2012.05.013 · Cited by 199
The role of oxidative stress in atherosclerosis.
Vogiatzi, G., Tousoulis, D., & Stefanadis, C. (2009) · PubMed · Cited by 197
Oxidative Stress and MicroRNAs in Vascular Diseases
Magenta, A., Greco, S., Gaetano, C., & Martelli, F. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms140917319 · Cited by 197
“It must be underlined that cardiovascular diseases are multifactorial, involving a complex interplay between lifestyle (smoking, diet, ethanol consumption, exercise) and fixed (age, genotype, menopausal status, sex) causative factors [11,12].”
BackgroundNeurovascular Dysfunction in Vascular Dementia, Alzheimer's and Atherosclerosis
Shabir, O., Berwick, J., & Francis, S. E. (2018) · BMC Neuroscience · doi:10.1186/s12868-018-0465-5 · Cited by 191
Silver, A., Beske, S. D., Christou, D. D., Donato, A. J., Moreau, K. L., Eskurza, I., Gates, P. E., & Seals, D. R. (2007) · Circulation · doi:10.1161/circulationaha.106.657486 · Cited by 190
Reactive oxygen species: influence on cerebral vascular tone
Faraci, F. M. (2006) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01044.2005 · Cited by 189
“There are multiple sources of superoxide within vascular cells, including mitochondria, cyclooxygenases, NAD(P)H oxidases, xanthine oxidases, lipoxygenases, and, under special circumstances, nitric oxide synthases (37, 42).”
BackgroundOxidant mechanisms in childhood obesity: the link between inflammation and oxidative stress
Codoñer‐Franch, P., Valls‐Bellés, V., Arilla-Codoñer, Á., & Alonso‐Iglesias, E. (2011) · Translational research · doi:10.1016/j.trsl.2011.08.004 · Cited by 189
Recent Advances in Understanding Endothelial Dysfunction in Atherosclerosis
Yang, Z., & Ming, X. (2006) · Clinical Medicine & Research · doi:10.3121/cmr.4.1.53 · Cited by 191
3D‐Printing Strong High‐Resolution Antioxidant Bioresorbable Vascular Stents
van Lith, R., Baker, E., Ware, H. O. T., Yang, J. H., Farsheed, A. C., Sun, C., & Ameer, G. A. (2016) · Advanced Materials Technologies · doi:10.1002/admt.201600138 · Cited by 189
Mechanosensitive TRP channels in cardiovascular pathophysiology
Inoue, R., Zhong, J., & Kawarabayashi, Y. (2009) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2009.05.009 · Cited by 199
“These changesmay be at least in part associated with altered expression and/or properties of ion channels regulating Ca homeostasis in response to growth signals and/or inflammatory signals, as well as to cellular stresses including oxidative and mechanical stresses (Madamanchi et al., 2005; Bers, 2006; Nattel et al.,…”
BackgroundBräunlich, M., Slimestad, R., Wangensteen, H., Brede, C., Malterud, K. E., & Barsett, H. (2013) · Nutrients · doi:10.3390/nu5030663 · Cited by 188
“Reactive oxygen species can be generated by the prooxidative enzyme, XO, and the peroxidative enzyme, 15-LO, in vascular cells [31].”
BackgroundEffects of hydrogen sulfide on homocysteine-induced oxidative stress in vascular smooth muscle cells
Sheng-kai, Y., Chang, T., Wang, H., Wu, L., Wang, R., & Meng, Q. H. (2006) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2006.10.058 · Cited by 187
The sirtuin family members SIRT1, SIRT3 and SIRT6: Their role in vascular biology and atherogenesis
Sosnowska, B., Mazidi, M., Penson, P. E., Gluba-Brzózka, A., Rysz, J., & Banach, M. (2017) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2017.08.027 · Cited by 188
Oxidative stress in patients with cardiovascular disease and chronic renal failure
Popolo, A., Autore, G., Pinto, A., & Marzocco, S. (2013) · Free Radical Research · doi:10.3109/10715762.2013.779373 · Cited by 185
Bachar, A., Scheffer, L., Schroeder, A. S., Nakamura, H. K., Cobb, L. J., Oh, Y. K., Lerman, L. O., Pagano, R. E., Cohen, P., & Lerman, A. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq191 · Cited by 182
Metadata
- Authors
- Madamanchi, N. R., Vendrov, A., & Runge, M. S.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2005-01
- Volume
- 25
- Issue
- 1
- Pages
- 29-38
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2109698138
- Cited by
- 1,618
- References
- 135
- Citations by year
- 2026: 47 · 2025: 46 · 2024: 42 · 2023: 53 · 2022: 61 · 2021: 62 · 2020: 73 · 2019: 73 · 2018: 57 · 2017: 75 · 2016: 78 · 2015: 105 · 2014: 111 · 2013: 104 · 2012: 95
- FWCI
- 7.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- oxidative stress, reactive oxygen species, atherosclerosis, vascular disease, cardiovascular disease, NADPH oxidase, xanthine oxidase, lipoxygenase, nitric oxide synthase uncoupling, vascular inflammation, atherogenesis, antioxidants, redox signaling, biomarkers, cardiovascular risk factors
- MeSH terms
- Animals, Humans, Vascular Diseases, Oxidative Stress
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