Cited by 195Redox biology and oxidative stressCardiac Ischemia and ReperfusionCardiomyopathy and Myosin Studies

Oxidative Stress and Sarcomeric Proteins

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Steinberg, Susan F.·2013·Circulation Research

Abstract

Oxidative stress accompanies a wide spectrum of clinically important cardiac disorders, including ischemia/reperfusion, diabetes mellitus, and hypertensive heart disease. Although reactive oxygen species (ROS) can activate signaling pathways that contribute to ischemic preconditioning and cardioprotection, high levels of ROS induce structural modifications of the sarcomere that impact on pump function and the pathogenesis of heart failure. However, the precise nature of the redox-dependent change in contractility is determined by the source/identity of the oxidant species, the level of oxidative stress, and the chemistry/position of oxidant-induced posttranslational modifications on individual proteins within the sarcomere. This review focuses on various ROS-induced posttranslational modifications of myofilament proteins (including direct oxidative modifications of myofilament proteins, myofilament protein phosphorylation by ROS-activated signaling enzymes, and myofilament protein cleavage by ROS-activated proteases) that have been implicated in the control of cardiac contractility.

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  • Increased oxidative stress causes modifications of all subcellular organelles, including oxidation of endoplasmic reticulum Ca2+-ATPase and contractile proteins, resulting in contractile dysfunction.

    “Increased oxidative stress causes modifications of all subcellular organelles, including oxidation of endoplasmic reticulum Ca2+-ATPase and contractile proteins (actin and myosin being the most important) resulting in contractile dysfunction (Steinberg 2013).”

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Authors
Steinberg, S. F.
Affiliations
Columbia University (US)
Corresponding author
Steinberg, Susan F.
Venue
Circulation Research
Published
2013-01-18
Volume
112
Issue
2
Pages
393-405
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2004677075
Cited by
195
References
102
Citations by year
2026: 10 · 2025: 11 · 2024: 18 · 2023: 14 · 2022: 13 · 2021: 10 · 2020: 11 · 2019: 20 · 2018: 15 · 2017: 15 · 2016: 18 · 2015: 11 · 2014: 20 · 2013: 7 · 2012: 1
FWCI
1.76
Type
journal article
Language
en
Open access
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL112388, HL-77860, R01HL077860, HL112388)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
Keywords
oxidative stress, sarcomeric proteins, myofilament proteins, reactive oxygen species, post-translational modification, protein phosphorylation, proteolytic cleavage, proteolytic enzymes, cardiac contractility, heart failure, ischemia-reperfusion, diabetes mellitus, hypertensive heart disease, cardioprotection, ischemic preconditioning
MeSH terms
Animals, Humans, Protein Kinases, Sarcomeres, Reactive Oxygen Species, Oxidative Stress, Troponin C

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