The Role of ROS in Atherosclerosis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 980

Special Issue Editor

Departments of Radiology & Medical Imaging and of Biochemistry & Molecular Genetics, University of Virginia, Charlottesville, VA, USA
Interests: molecular and genetic determinants of atherosclerosis; cardiometabolic disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Atherosclerosis is a chronic inflammatory disease characterized by the buildup of fatty substances in the arterial walls, leading to heart attack, ischemic stroke, and gangrene. Despite optimal treatment with drugs to alleviate hypercholesterolemia, hypertension and type 2 diabetes, and prevent thrombotic complications, this disease continues to be the leading cause of death globally. Therefore, there is an urgent need for understanding the pathogenesis of atherosclerosis and finding more effective prevention and treatment strategies. Reactive oxygen/nitrogen species (ROS) are reactive intermediates of oxygen and nitrogen produced from various metabolic processes in various cells and are involved in essential biological processes. Oxidative stress resulting from an increased production of ROS and/or reduced antioxidant capacity is an important mechanism underlying the pathogenesis of many common diseases, including atherosclerosis. Traditional risk factors of atherosclerosis, such as dyslipidemia, hypertension, obesity, type 2 diabetes, smoking, and ageing, are major drivers of oxidative stress. There is considerable interest in the utilization of antioxidant molecules to treat atherosclerosis. In this Special Issue, we will consider both original and review articles that focus on role of ROS in atherosclerosis. We look forward to receiving your contributions.

Dr. Weibin Shi
Guest Editor

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Keywords

  • atherosclerosis
  • coronary artery disease
  • reactive oxygen species (ROS)
  • reactive nitrogen species (RNS)
  • free radical
  • oxidative stress
  • antioxidant
  • lipid peroxidation
  • inflammation

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Published Papers (1 paper)

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Research

23 pages, 1690 KiB  
Article
Comparative Analysis of Plasma Protein Dynamics in Women with ST-Elevation Myocardial Infarction and Takotsubo Syndrome
by Shafaat Hussain, Sandeep Jha, Evelin Berger, Linnea Molander, Valentyna Sevastianova, Zahra Sheybani, Aaron Shekka Espinosa, Ahmed Elmahdy, Amin Al-Awar, Yalda Kakaei, Mana Kalani, Ermir Zulfaj, Amirali Nejat, Abhishek Jha, Tetiana Pylova, Maryna Krasnikova, Erik Axel Andersson, Elmir Omerovic and Björn Redfors
Cells 2024, 13(21), 1764; https://doi.org/10.3390/cells13211764 - 24 Oct 2024
Viewed by 640
Abstract
Background: ST-elevation myocardial infarction (STEMI) and Takotsubo syndrome (TS) are two distinct cardiac conditions that both result in sudden loss of cardiac dysfunction and that are difficult to distinguish clinically. This study compared plasma protein changes in 24 women with STEMI and 12 [...] Read more.
Background: ST-elevation myocardial infarction (STEMI) and Takotsubo syndrome (TS) are two distinct cardiac conditions that both result in sudden loss of cardiac dysfunction and that are difficult to distinguish clinically. This study compared plasma protein changes in 24 women with STEMI and 12 women with TS in the acute phase (days 0–3 post symptom onset) and the stabilization phase (days 7, 14, and 30) to examine the molecular differences between these conditions. Methods: Plasma proteins from STEMI and TS patients were extracted during the acute and stabilization phases and analyzed via quantitative proteomics. Differential expression and functional significance were assessed. Data are accessible on ProteomeXchange, ID PXD051367. Results: During the acute phase, STEMI patients showed higher levels of myocardial inflammation and tissue damage proteins compared to TS patients, along with reduced tissue repair and anti-inflammatory proteins. In the stabilization phase, STEMI patients exhibited ongoing inflammation and disrupted lipid metabolism. Notably, ADIPOQ was consistently downregulated in STEMI patients in both phases. When comparing the acute to the stabilization phase, STEMI patients showed increased inflammatory proteins and decreased structural proteins. Conversely, TS patients showed increased proteins involved in inflammation and the regulatory response to counter excessive inflammation. Consistent protein changes between the acute and stabilization phases in both conditions, such as SAA2, CRP, SAA1, LBP, FGL1, AGT, MAN1A1, APOA4, COMP, and PCOLCE, suggest shared underlying pathophysiological mechanisms. Conclusions: This study presents protein changes in women with STEMI or TS and identifies ADIPOQ, SAA2, CRP, SAA1, LBP, FGL1, AGT, MAN1A1, APOA4, COMP, and PCOLCE as candidates for further exploration in both therapeutic and diagnostic contexts. Full article
(This article belongs to the Special Issue The Role of ROS in Atherosclerosis)
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