ArticleJournal of physiology and biochemistry2019
Tyrosine nitration of mitochondrial proteins during myocardial ischemia and reperfusion.
Article in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Proteomics of the heart.Physiological reviews · 2024Review
- Age-Dependent Changes in Calcium Regulation after Myocardial Ischemia-Reperfusion Injury.Biomedicines · 2023Article
- Proteomics as a Tool for the Study of Mitochondrial Proteome, Its Dysfunctionality and Pathological Consequences in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Effect of hyperhomocysteinemia on rat cardiac sarcoplasmic reticulum.Molecular and cellular biochemistry · 2022Article
- Data-independent acquisition proteomics reveals circulating biomarkers of coronary chronic total occlusion in humans.Frontiers in cardiovascular medicine · 2022Article
- Melatonin, Its Metabolites and Their Interference with Reactive Nitrogen Compounds.Molecules (Basel, Switzerland) · 2021Review
- Uncommon posttranslational modifications in proteomics: ADP-ribosylation, tyrosine nitration, and tyrosine sulfation.Mass spectrometry reviewsReview
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial ischemia reperfusion is associated with mitochondrial dysfunction and increased formation of reactive oxygen/nitrogen species. The main purpose of this study was to assess the role of tyrosine nitration of mitochondrial proteins in postischemic contractile dysfunction known as myocardial stunning. Isolated Langendorff-perfused rat hearts were subjected to 20-min global ischemia followed by 30-min reperfusion. The reperfused hearts showed marked decline in left ventricular developed pressure, maximal rate of contraction (+dP/dt), and maximal rate of relaxation (-dP/dt). Immunofluorescence and ELISA assays demonstrated enhanced protein tyrosine nitration in reperfused hearts. Using two-dimensional gel electrophoresis and MALDI-TOF/TOF mass spectrometry, eight mitochondrial proteins were identified to be nitrated after ischemia reperfusion. These proteins are crucial in mitochondrial electron transport, fatty acid oxidation, tricarboxylic acid cycle, ATP synthesis, and control of high-energy phosphates. The proteome data also indicated reduced abundance in several of nitrated proteins. The results suggest that these changes may contribute to inhibition of aconitase activity but are unlikely to affect electron transport chain activity. Whether tyrosine nitration of mitochondrial proteins can be considered the contributing factor of postischemic contractile dysfunction remains to be explored.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.