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Antioxidants
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Protein Lipoxidation at the Crossroads between Reactive Lipid Species and...
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Protein Lipoxidation at the Crossroads between Reactive Lipid Species and Redox Signaling

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Aberrant Oxidation of Biomolecules".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 3825

Special Issue Editors

Dr. Dolores Pérez-Sala

E-Mail Website
Guest Editor
Department of Structural and Chemical Biology, Centro de Investigaciones Biológicas Margarita Salas, CSIC, 28040 Madrid, Spain
Interests: protein lipoxidation; protein posttranslational modification; redox signaling; cysteine modifica-tions; intermediate filaments; redox sensors
Dr. Maria do Rosário Domingues

E-Mail Website
Guest Editor
CESAM, Department of Chemistry, University of Aveiro, Campus Universitario de Santiago, 3810-193 Aveiro, Portugal
Interests: lipidomics; oxidized lipids; nitrated/nitroxidized lipids; protein lipoxidation; Mass spectrometry; LC-MS
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Lipids are key components of cellular membranes and important signaling molecules. From their synthesis, lipids are subjected to numerous modifications that lead to an amazing variety of molecules with diverse functions. Some transformations occurring in the presence of free radicals, for instance, in situations associated with oxidative and/or nitrative/nitroxidative stress, such as inflammation or neurodegeneration, lead to the formation of reactive lipid species (e.g., electrophilic oxidized lipids, nitro-lipids) that are able to covalently bind to other macromolecules, including other lipids, DNA, and proteins. The covalent modification of proteins by these electrophilic lipids is known as protein lipoxidation. Protein lipoxidation, although often widespread in cells or tissues, is not a random process but occurs preferentially in certain protein targets and residues. Nucleophilic residues in proteins, including cysteine, histidine, and lysine, are the most frequent targets of lipoxidation. Although initially considered a damaging mechanism, it is becoming clear that protein lipoxidation can also have signaling functions and/or contribute to cellular adaptation to stress. The great structural variety of the lipid moieties involved in protein lipoxidation can lead to a great diversity of proteoforms, thus increasing the structural and functional outcomes of protein modification. Moreover, recently proposed mechanisms for reversibility call attention to the potential regulatory capacity of some types of lipoxidation. In addition, there can be crosstalk and/or interplay of lipoxidation and other posttranslational modifications affecting the target residues. Protein lipoxidation can influence the activity of redox-sensitive protein phosphatases, as well as of key proteins involved in redox regulation, thus contributing to a complex landscape of protein modifications.

The present Special Issue aims to collect articles dealing with cutting-edge aspects of protein lipoxidation, including the generation of electrophilic lipids, structural and functional studies of protein targets, analytical challenges related to these processes, importance in physiology and pathophysiology, possibilities for regulation, interplay with other protein modifications, and perspectives for therapeutic intervention.

Dr. Dolores Pérez-Sala
Dr. Maria do Rosário Domingues
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • protein lipoxidation
  • oxidative/nitroxidative stress
  • electrophilic lipids
  • epilipidomics
  • redox sig-naling
  • posttranslational modifications
  • cysteine modifications interplay
  • pathophysiology

Published Papers (3 papers)

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Research

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16 pages, 1425 KiB  
Article
High-Fat Diet-Induced Obesity Increases Brain Mitochondrial Complex I and Lipoxidation-Derived Protein Damage
by Rebeca Berdún, Èlia Obis, Natàlia Mota-Martorell, Anna Bassols, Daniel Valent, José C. E. Serrano, Meritxell Martín-Garí, María Rodríguez-Palmero, José Antonio Moreno-Muñoz, Joan Tibau, Raquel Quintanilla, Reinald Pamplona, Manuel Portero-Otín and Mariona Jové
Antioxidants 2024, 13(2), 161; https://doi.org/10.3390/antiox13020161 - 26 Jan 2024
Viewed by 1010
Abstract
Obesity is a risk factor for highly prevalent age-related neurodegenerative diseases, the pathogenesis of whichinvolves mitochondrial dysfunction and protein oxidative damage. Lipoxidation, driven by high levels of peroxidizable unsaturated fatty acids and low antioxidant protection of the brain, stands out as a significant [...] Read more.
Obesity is a risk factor for highly prevalent age-related neurodegenerative diseases, the pathogenesis of whichinvolves mitochondrial dysfunction and protein oxidative damage. Lipoxidation, driven by high levels of peroxidizable unsaturated fatty acids and low antioxidant protection of the brain, stands out as a significant risk factor. To gain information on the relationship between obesity and brain molecular damage, in a porcine model of obesity we evaluated (1) the level of mitochondrial respiratory chain complexes, as the main source of free radical generation, by Western blot; (2) the fatty acid profile by gas chromatography; and (3) the oxidative modification of proteins by mass spectrometry. The results demonstrate a selectively higher amount of the lipoxidation-derived biomarker malondialdehyde-lysine (MDAL) (34% increase) in the frontal cortex, and positive correlations between MDAL and LDL levels and body weight. No changes were observed in brain fatty acid profile by the high-fat diet, and the increased lipid peroxidative modification was associated with increased levels of mitochondrial complex I (NDUFS3 and NDUFA9 subunits) and complex II (flavoprotein). Interestingly, introducing n3 fatty acids and a probiotic in the high-fat diet prevented the observed changes, suggesting that dietary components can modulate protein oxidative modification at the cerebral level and opening new possibilities in neurodegenerative diseases’ prevention. Full article
(This article belongs to the Special Issue Protein Lipoxidation at the Crossroads between Reactive Lipid Species and Redox Signaling)
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22 pages, 5435 KiB  
Article
Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue
by Diego Moneo-Corcuera, Álvaro Viedma-Poyatos, Konstantinos Stamatakis and Dolores Pérez-Sala
Antioxidants 2023, 12(9), 1703; https://doi.org/10.3390/antiox12091703 - 31 Aug 2023
Cited by 2 | Viewed by 1015
Abstract
The type III intermediate filament proteins vimentin and GFAP are modulated by oxidants and electrophiles, mainly through perturbation of their single cysteine residues. Desmin, the type III intermediate filament protein specific to muscle cells, is critical for muscle homeostasis, playing a key role [...] Read more.
The type III intermediate filament proteins vimentin and GFAP are modulated by oxidants and electrophiles, mainly through perturbation of their single cysteine residues. Desmin, the type III intermediate filament protein specific to muscle cells, is critical for muscle homeostasis, playing a key role in sarcomere organization and mitochondrial function. Here, we have studied the impact of oxidants and cysteine-reactive agents on desmin behavior. Our results show that several reactive species and drugs induce covalent modifications of desmin in vitro, of which its single cysteine residue, C333, is an important target. Moreover, stimuli eliciting oxidative stress or lipoxidation, including H2O2, 15-deoxy-prostaglandin J2, and CoCl2-elicited chemical hypoxia, provoke desmin disorganization in H9c2 rat cardiomyoblasts transfected with wild-type desmin, which is partially attenuated in cells expressing a C333S mutant. Notably, in cells lacking other cytoplasmic intermediate filaments, network formation by desmin C333S appears less efficient than that of desmin wt, especially when these proteins are expressed as fluorescent fusion constructs. Nevertheless, in these cells, the desmin C333S organization is also protected from disruption by oxidants. Taken together, our results indicate that desmin is a target for oxidative and electrophilic stress, which elicit desmin remodeling conditioned by the presence of its single cysteine residue. Full article
(This article belongs to the Special Issue Protein Lipoxidation at the Crossroads between Reactive Lipid Species and Redox Signaling)
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Review

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26 pages, 1247 KiB  
Review
Reactive Carbonyl Species and Protein Lipoxidation in Atherogenesis
by Anne Nègre-Salvayre and Robert Salvayre
Antioxidants 2024, 13(2), 232; https://doi.org/10.3390/antiox13020232 - 14 Feb 2024
Viewed by 1099
Abstract
Atherosclerosis is a multifactorial disease of medium and large arteries, characterized by the presence of lipid-rich plaques lining the intima over time. It is the main cause of cardiovascular diseases and death worldwide. Redox imbalance and lipid peroxidation could play key roles in [...] Read more.
Atherosclerosis is a multifactorial disease of medium and large arteries, characterized by the presence of lipid-rich plaques lining the intima over time. It is the main cause of cardiovascular diseases and death worldwide. Redox imbalance and lipid peroxidation could play key roles in atherosclerosis by promoting a bundle of responses, including endothelial activation, inflammation, and foam cell formation. The oxidation of polyunsaturated fatty acids generates various lipid oxidation products such as reactive carbonyl species (RCS), including 4-hydroxy alkenals, malondialdehyde, and acrolein. RCS covalently bind to nucleophilic groups of nucleic acids, phospholipids, and proteins, modifying their structure and activity and leading to their progressive dysfunction. Protein lipoxidation is the non-enzymatic post-translational modification of proteins by RCS. Low-density lipoprotein (LDL) oxidation and apolipoprotein B (apoB) modification by RCS play a major role in foam cell formation. Moreover, oxidized LDLs are a source of RCS, which form adducts on a huge number of proteins, depending on oxidative stress intensity, the nature of targets, and the availability of detoxifying systems. Many systems are affected by lipoxidation, including extracellular matrix components, membranes, cytoplasmic and cytoskeletal proteins, transcription factors, and other components. The mechanisms involved in lipoxidation-induced vascular dysfunction are not fully elucidated. In this review, we focus on protein lipoxidation during atherogenesis. Full article
(This article belongs to the Special Issue Protein Lipoxidation at the Crossroads between Reactive Lipid Species and Redox Signaling)
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