Oxidation of cardiac myofilament proteins: Priming for dysfunction?
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Oxidation of cardiac myofilament proteins: Priming for dysfunction? / Cuello, Friederike; Wittig, Ilka; Lorenz, Kristina; Eaton, Philip.
in: MOL ASPECTS MED, Jahrgang 63, Nr. SI, 10.2018, S. 47-58.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Oxidation of cardiac myofilament proteins: Priming for dysfunction?
AU - Cuello, Friederike
AU - Wittig, Ilka
AU - Lorenz, Kristina
AU - Eaton, Philip
N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.
PY - 2018/10
Y1 - 2018/10
N2 - Oxidants are produced endogenously and can react with and thereby post-translationally modify target proteins. They have been implicated in the redox regulation of signal transduction pathways conferring protection, but also in mediating oxidative stress and causing damage. The difference is that in scenarios of injury the amount of oxidants generated is higher and/or the duration of oxidant exposure sustained. In the cardiovascular system, oxidants are important for blood pressure homeostasis, for unperturbed cardiac function and also contribute to the observed protection during ischemic preconditioning. In contrast, oxidative stress accompanies all major cardiovascular pathologies and has been attributed to mediate contractile dysfunction in part by inducing oxidative modifications in myofilament proteins. However, the proportion to which oxidative modifications of contractile proteins are beneficial or causatively mediate disease progression needs to be carefully reconsidered. These antithetical aspects will be discussed in this review with special focus on direct oxidative post-translational modifications of myofilament proteins that have been described to occur in vivo and to regulate actin-myosin interactions in the cardiac myocyte sarcomere, the methodologies for detection of oxidative post-translational modifications in target proteins and the feasibility of antioxidant therapy strategies as a potential treatment for cardiac disorders.
AB - Oxidants are produced endogenously and can react with and thereby post-translationally modify target proteins. They have been implicated in the redox regulation of signal transduction pathways conferring protection, but also in mediating oxidative stress and causing damage. The difference is that in scenarios of injury the amount of oxidants generated is higher and/or the duration of oxidant exposure sustained. In the cardiovascular system, oxidants are important for blood pressure homeostasis, for unperturbed cardiac function and also contribute to the observed protection during ischemic preconditioning. In contrast, oxidative stress accompanies all major cardiovascular pathologies and has been attributed to mediate contractile dysfunction in part by inducing oxidative modifications in myofilament proteins. However, the proportion to which oxidative modifications of contractile proteins are beneficial or causatively mediate disease progression needs to be carefully reconsidered. These antithetical aspects will be discussed in this review with special focus on direct oxidative post-translational modifications of myofilament proteins that have been described to occur in vivo and to regulate actin-myosin interactions in the cardiac myocyte sarcomere, the methodologies for detection of oxidative post-translational modifications in target proteins and the feasibility of antioxidant therapy strategies as a potential treatment for cardiac disorders.
KW - Journal Article
KW - Review
U2 - 10.1016/j.mam.2018.08.003
DO - 10.1016/j.mam.2018.08.003
M3 - SCORING: Review article
C2 - 30130564
VL - 63
SP - 47
EP - 58
JO - MOL ASPECTS MED
JF - MOL ASPECTS MED
SN - 0098-2997
IS - SI
ER -