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Cited by 103Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionAutophagy in Disease and Therapy

The DOI matches its Crossref record; 69 of the 69 references it cites were found in a registry or an index.

Elucidating Mitochondrial Electron Transport Chain Supercomplexes in the Heart During Ischemia–Reperfusion

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Jang, Sehwan, Lewis, Taber S., Powers, Corey, Khuchua, Zaza, Baines, Christopher P., Wipf, Peter, Javadov, Sabzali·2017·Antioxidants & Redox Signaling
DOI 10.1089/ars.2016.6635PMC PMC5488255
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Abstract

AIMS: Mitochondrial supercomplexes (SCs) are the large supramolecular assembly of individual electron transport chain (ETC) complexes that apparently provide highly efficient ATP synthesis and reduce electron leakage and reactive oxygen species (ROS) production. Oxidative stress during cardiac ischemia-reperfusion (IR) can result in degradation of SCs through oxidation of cardiolipin (CL). Also, IR induces calcium overload and enhances reactive oxygen species (mitROS) in mitochondria that result in the opening of the nonselective permeability transition pores (PTP). The opening of the PTP further compromises cellular energetics and increases mitROS ultimately leading to cell death. Here, we examined the role of PTP-induced mitROS in disintegration of SCs during cardiac IR. The relationship between mitochondrial PTP, ROS, and SCs was investigated using Langendorff-perfused rat hearts subjected to global ischemia (25 min) followed by short-time (5 min) or long-time (60 min) reperfusion in the presence or absence of the PTP inhibitor, sanglifehrin A (SfA), and the mitochondrial targeted ROS and electron scavenger, XJB-5-131. Also, the effects of CL deficiency on SC degradation, PTP, and mitROS were investigated in tafazzin knockdown (TazKD) mice. RESULTS: Cardiac IR induced PTP opening and mitROS generation, inhibited by SfA. Percent distributions of SCs were significantly affected by IR, and the effects were dependent on the reperfusion time and reversed by SfA and XJB-5-131. TazKD mice demonstrated a 40% lower SC I + III+IV with reduced basal mitochondrial PTP, ROS, and ETC complex activity. Innovation and Conclusion: Sustained reperfusion after cardiac ischemia induces disintegration of mitochondrial SCs, and PTP-induced ROS presumably play a causal role in SC disassembly. Antioxid. Redox Signal. 27, 57-69.

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Metadata

Authors
Jang, S., Lewis, T. S., Powers, C., Khuchua, Z., Baines, C. P., Wipf, P., & Javadov, S.
Affiliations
  • University of Puerto Rico, Medical Sciences Campus (PR)
  • University of Pittsburgh (US)
  • Cincinnati Children's Hospital Medical Center (US)
  • University of Missouri (US)
Corresponding author
Javadov, Sabzali
ORCID
Venue
Antioxidants & Redox Signaling
Publisher
SAGE Publications
Published
2017-07
Volume
27
Issue
1
Pages
57-69
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
DOI
10.1089/ars.2016.6635
PMC
PMC5488255
OpenAlex
W2556127230
Cited by
103
References
69
Citations by year
2026: 5 · 2025: 11 · 2024: 14 · 2023: 7 · 2022: 11 · 2021: 10 · 2020: 9 · 2019: 10 · 2018: 11 · 2017: 15
FWCI
6.23
Type
journal article
Language
en
Open access
Licence
www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/ (tdm)
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL094404, SC1HL118669, R01HL108867)
  • National Center for Research Resources (G12RR003051)
  • National Institute on Minority Health and Health Disparities (G12MD007600)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords
mitochondrial supercomplexes, electron transport chain, cardiac ischemia-reperfusion, mitochondrial permeability transition pore, mitochondrial reactive oxygen species, cardiolipin, tafazzin, sanglifehrin A, oxidative stress, calcium overload, mitochondrial dysfunction
MeSH terms
Mitochondrial Permeability Transition Pore, Animals, Cyclic N-Oxides, Disease Models, Animal, Electron Transport, Female, Lactones, Male, Mitochondria, Heart, Spiro Compounds, Myocardial Reperfusion Injury, Reactive Oxygen Species, Oxidative Stress, Mitochondrial Membrane Transport Proteins, Rats

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