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Review
. 2020 Sep 14;9(9):864.
doi: 10.3390/antiox9090864.

Oxidative Stress in Cardiovascular Diseases

Emilie Dubois-Deruy  1 , Victoriane Peugnet  1 , Annie Turkieh  1 , Florence Pinet  1
Affiliations
Review

Oxidative Stress in Cardiovascular Diseases

Emilie Dubois-Deruy et al. Antioxidants (Basel). .

Abstract

Reactive oxygen species (ROS) are subcellular messengers in signal transductions pathways with both beneficial and deleterious roles. ROS are generated as a by-product of mitochondrial respiration or metabolism or by specific enzymes such as superoxide dismutases, glutathione peroxidase, catalase, peroxiredoxins, and myeloperoxidases. Under physiological conditions, the low levels of ROS production are equivalent to their detoxification, playing a major role in cellular signaling and function. In pathological situations, particularly atherosclerosis or hypertension, the release of ROS exceeds endogenous antioxidant capacity, leading to cell death. At cardiovascular levels, oxidative stress is highly implicated in myocardial infarction, ischemia/reperfusion, or heart failure. Here, we will first detail the physiological role of low ROS production in the heart and the vessels. Indeed, ROS are able to regulate multiple cardiovascular functions, such as cell proliferation, migration, and death. Second, we will investigate the implication of oxidative stress in cardiovascular diseases. Then, we will focus on ROS produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction. Given the importance of oxidative stress at the cardiovascular level, antioxidant therapies could be a real benefit. In the last part of this review, we will detail the new therapeutic strategies potentially involved in cardiovascular protection and currently under study.

Keywords: antioxidant; cardiovascular diseases; kinase; mitochondria; oxidative stress; reactive oxygen species.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
ROS formation and detoxification. 1O2: singlet oxygen; Cl−: chloride ion; Fe2+: iron (II) ion; Fe3+: iron (III) ion; GPX: glutathione peroxidase; H+: proton; H2O: water; H2O2: hydrogen peroxide; HOCl: hypochlorous acid; MPO: myeloperoxidases; NO: nitric oxide; O2: dioxygen; ●O2−: superoxide anion; ●OH: hydroxyl radical; ONOO-: peroxynitrite; ONOOH: peroxynitrous acid; Prx: peroxiredoxins; SOD: superoxide dismutases.
Figure 2
Figure 2
Compartmentalization of cardiac antioxidant enzymes. C: cytosol; EC: Extracellular compartment; L: lysosomes; M: mitochondria; N: nucleus; GPX 1–4: glutathione peroxidase 1–4; SOD 1–3: superoxide dismutase 1–3; Txn 1–2: thioredoxin 1 and 2; Trx 1–2: thioredoxin reductase 1 and 2; MPO: myeloperoxidase; Prx 1–6: peroxiredoxin 1–6.
Figure 3
Figure 3
Physiological roles of oxidative stress in cardiovascular tissues. Black arrow represents activation and red arrow represents inhibition. p38 MAPK: p38 mitogen-activated protein kinase; JNK: c-Jun N-terminal kinase; H2O2: hydrogen peroxide; NFκB: nuclear factor-kappa beta; CAMKII: Ca/calmodulin-dependent kinase II; RyR: ryanodine receptor; PKA: cAMP-induced protein kinase A; NO: nitric oxide; PKG: protein kinase G; Nrf2: nuclear factor erythroid 2-related factor 2.
Figure 4
Figure 4
Pathological roles of oxidative stress in cardiovascular tissues. ROS: reactive oxygen species; NOS: nitric oxide synthase; mtDNA: mitochondrial DNA; JNK: c-Jun N-terminal kinase; Erk1/2: Extracellular signal-regulated kinases; p38 MAPK: p38 mitogen-activated protein kinase; CAMKII: Ca/calmodulin-dependent kinase II.
See this image and copyright information in PMC

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