Oxidative Stress and Sarcomeric Proteins
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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).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Steinberg 2013
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Impact of Actin Glutathionylation on the Actomyosin-S1 ATPase
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Peroxynitrite-induced cardiac depression: role of myofilament desensitization and cGMP pathway
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Raf-1: a novel cardiac troponin T kinase
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Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging
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Mitochondrial and cellular mechanisms for managing lipid excess
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ROS signaling and redox biology in endothelial cells
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Fundamental mechanisms of the cell death caused by Nitrosative stress
Wang, F., Yuan, Q., Chen, F., Pang, J., Pan, C., Xu, F., & Chen, Y. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.742483 · Cited by 133 · see citing works
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Reactive oxygen species in the pathogenesis of sarcopenia
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Human heart disease: lessons from human pluripotent stem cell-derived cardiomyocytes
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- Authors
- Steinberg, S. F.
- Affiliations
- Columbia University (US)
- Corresponding author
- Steinberg, Susan F.
- ORCID
- Steinberg, Susan F.
- Venue
- Circulation Research
- Published
- 2013-01-18
- Volume
- 112
- Issue
- 2
- Pages
- 393-405
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC3595003
- 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
- bronze
- doi.org
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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