CVD and Oxidative Stress

Overview

Journal J Clin Med

Specialty General Medicine

Date 2017 Feb 24

PMID 28230726

Citations 132

Authors

Karla Cervantes Gracia

Daniel Llanas-Cornejo

Holger Husi

Affiliations

Soon will be listed here.

Abstract

Nowadays, it is known that oxidative stress plays at least two roles within the cell, the generation of cellular damage and the involvement in several signaling pathways in its balanced normal state. So far, a substantial amount of time and effort has been expended in the search for a clear link between cardiovascular disease (CVD) and the effects of oxidative stress. Here, we present an overview of the different sources and types of reactive oxygen species in CVD, highlight the relationship between CVD and oxidative stress and discuss the most prominent molecules that play an important role in CVD pathophysiology. Details are given regarding common pharmacological treatments used for cardiovascular distress and how some of them are acting upon ROS-related pathways and molecules. Novel therapies, recently proposed ROS biomarkers, as well as future challenges in the field are addressed. It is apparent that the search for a better understanding of how ROS are contributing to the pathophysiology of CVD is far from over, and new approaches and more suitable biomarkers are needed for the latter to be accomplished.

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References

Martin-Garrido A, Brown D, Lyle A, Dikalova A, Seidel-Rogol B, Lassegue B . NADPH oxidase 4 mediates TGF-β-induced smooth muscle α-actin via p38MAPK and serum response factor. Free Radic Biol Med. 2010; 50(2):354-62. PMC: 3032946. DOI: 10.1016/j.freeradbiomed.2010.11.007. View

Ebrahimian T, Li M, Lemarie C, Simeone S, Pagano P, Gaestel M . Mitogen-activated protein kinase-activated protein kinase 2 in angiotensin II-induced inflammation and hypertension: regulation of oxidative stress. Hypertension. 2010; 57(2):245-54. PMC: 4521212. DOI: 10.1161/HYPERTENSIONAHA.110.159889. View

Mittal C, Murad F . Activation of guanylate cyclase by superoxide dismutase and hydroxyl radical: a physiological regulator of guanosine 3',5'-monophosphate formation. Proc Natl Acad Sci U S A. 1977; 74(10):4360-4. PMC: 431941. DOI: 10.1073/pnas.74.10.4360. View

Madungwe N, Zilberstein N, Feng Y, Bopassa J . Critical role of mitochondrial ROS is dependent on their site of production on the electron transport chain in ischemic heart. Am J Cardiovasc Dis. 2016; 6(3):93-108. PMC: 5030389. View

Ago T, Kuroda J, Pain J, Fu C, Li H, Sadoshima J . Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes. Circ Res. 2010; 106(7):1253-64. PMC: 2855780. DOI: 10.1161/CIRCRESAHA.109.213116. View

Di Lisa F, Bernardi P . A CaPful of mechanisms regulating the mitochondrial permeability transition. J Mol Cell Cardiol. 2009; 46(6):775-80. DOI: 10.1016/j.yjmcc.2009.03.006. View

Doughan A, Harrison D, Dikalov S . Molecular mechanisms of angiotensin II-mediated mitochondrial dysfunction: linking mitochondrial oxidative damage and vascular endothelial dysfunction. Circ Res. 2007; 102(4):488-96. DOI: 10.1161/CIRCRESAHA.107.162800. View

Norton C, Broughton B, Jernigan N, Walker B, Resta T . Enhanced depolarization-induced pulmonary vasoconstriction following chronic hypoxia requires EGFR-dependent activation of NAD(P)H oxidase 2. Antioxid Redox Signal. 2012; 18(14):1777-88. PMC: 3619151. DOI: 10.1089/ars.2012.4836. View

Funk C . Leukotriene modifiers as potential therapeutics for cardiovascular disease. Nat Rev Drug Discov. 2005; 4(8):664-72. DOI: 10.1038/nrd1796. View

10.

Bedard K, Jaquet V, Krause K . NOX5: from basic biology to signaling and disease. Free Radic Biol Med. 2011; 52(4):725-34. DOI: 10.1016/j.freeradbiomed.2011.11.023. View

11.

Sorescu D, Weiss D, Lassegue B, Clempus R, Szocs K, Sorescu G . Superoxide production and expression of nox family proteins in human atherosclerosis. Circulation. 2002; 105(12):1429-35. DOI: 10.1161/01.cir.0000012917.74432.66. View

12.

Baldus S, Rudolph V, Roiss M, Ito W, Rudolph T, Eiserich J . Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidase. Circulation. 2006; 113(15):1871-8. DOI: 10.1161/CIRCULATIONAHA.105.590083. View

13.

Judkins C, Diep H, Broughton B, Mast A, Hooker E, Miller A . Direct evidence of a role for Nox2 in superoxide production, reduced nitric oxide bioavailability, and early atherosclerotic plaque formation in ApoE-/- mice. Am J Physiol Heart Circ Physiol. 2009; 298(1):H24-32. DOI: 10.1152/ajpheart.00799.2009. View

14.

Givertz M, Mann D, Lee K, Ibarra J, Velazquez E, Hernandez A . Xanthine oxidase inhibition for hyperuricemic heart failure patients: design and rationale of the EXACT-HF study. Circ Heart Fail. 2013; 6(4):862-8. PMC: 3902033. DOI: 10.1161/CIRCHEARTFAILURE.113.000394. View

15.

Mandal D, Fu P, Levine A . RETRACTED: REDOX regulation of IL-13 signaling in intestinal epithelial cells: usage of alternate pathways mediates distinct gene expression patterns. Cell Signal. 2010; 22(10):1485-94. PMC: 3006087. DOI: 10.1016/j.cellsig.2010.05.017. View

16.

Konior A, Schramm A, Czesnikiewicz-Guzik M, Guzik T . NADPH oxidases in vascular pathology. Antioxid Redox Signal. 2013; 20(17):2794-814. PMC: 4026218. DOI: 10.1089/ars.2013.5607. View

17.

Vendrov A, Vendrov K, Smith A, Yuan J, Sumida A, Robidoux J . NOX4 NADPH Oxidase-Dependent Mitochondrial Oxidative Stress in Aging-Associated Cardiovascular Disease. Antioxid Redox Signal. 2015; 23(18):1389-409. PMC: 4692134. DOI: 10.1089/ars.2014.6221. View

18.

Jensen P . Antimycin-insensitive oxidation of succinate and reduced nicotinamide-adenine dinucleotide in electron-transport particles. I. pH dependency and hydrogen peroxide formation. Biochim Biophys Acta. 1966; 122(2):157-66. DOI: 10.1016/0926-6593(66)90057-9. View

19.

Patterson C, Van der Merwe M, Hu Z, Holland S, Yeh E, Runge M . p47phox is required for atherosclerotic lesion progression in ApoE(-/-) mice. J Clin Invest. 2001; 108(10):1513-22. PMC: 209414. DOI: 10.1172/JCI11927. View

20.

Gao L, Mann G . Vascular NAD(P)H oxidase activation in diabetes: a double-edged sword in redox signalling. Cardiovasc Res. 2009; 82(1):9-20. DOI: 10.1093/cvr/cvp031. View