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Antioxidants
Special Issues
Oxidative Stress in Metabolic Syndrome and Cardiovascular Diseases
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Oxidative Stress in Metabolic Syndrome and Cardiovascular Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 4991

Special Issue Editors

Dr. Anna Wai San Cheang

E-Mail Website
Guest Editor
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR 999078, China
Interests: natural products; vascular diseases; metabolic disorders; pharmacology; biological activity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Cheng-Chao Ruan

E-Mail Website
Guest Editor
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200437, China
Interests: cardiovascular diseases; inflammation; obesity; hypertension; adipose tissue dysfunction; immunity

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) such as superoxide anion and hydrogen peroxide at regulated levels play physiological functions by maintaining normal cellular redox signaling. By contrast, a disturbed balance between ROS production and detoxification of reactive intermediates results in excessive oxidative stress. Various mechanisms, including mitochondrial dysfunction, excessive glycolytic metabolism, activation of the innate and adaptive inflammatory responses, endoplasmic reticulum stress and hypoxia, can lead to oxidative stress. Cellular generation of ROS and oxidative damage are associated with the development and progression of the metabolic syndrome and cardiovascular diseases such as hypertension, atherosclerosis, myocardial infarction and heart failure.

Evaluating the role of oxidative stress in dysregulation of redox-sensitive biological pathways in metabolic and cardiovascular diseases is an area of great interest, so as to increase knowledge and lead to the development of innovative approaches to counteracting excess oxidative stress to improve or avoid oxidative stress-related effects. This Special Issue calls for original research and full reviews that address the progress and provide novel findings on the importance of oxidative stress in the pathophysiology of diseases and new therapeutic strategies.

Contributions need not be limited to the fields mentioned in the keywords. We look forward to your contributions.

Dr. Anna Wai San Cheang
Prof. Dr. Cheng-Chao Ruan
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

  • oxidative stress
  • metabolic disorders
  • cardiovascular diseases
  • antioxidant therapeutic strategies
  • natural and chemical antioxidants

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Published Papers (2 papers)

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17 pages, 4016 KiB  
Article
Portulaca Oleracea L. (Purslane) Extract Protects Endothelial Function by Reducing Endoplasmic Reticulum Stress and Oxidative Stress through AMPK Activation in Diabetic Obese Mice
by Lingchao Miao, Chunxiu Zhou, Haolin Zhang, Meng Sam Cheong, Yi Tan, Yuehan Wang, Xutao Zhang, Hua Yu and Wai San Cheang
Antioxidants 2023, 12(12), 2132; https://doi.org/10.3390/antiox12122132 - 18 Dec 2023
Cited by 1 | Viewed by 2042
Abstract
Portulaca oleracea L. (purslane) is a food and a traditional drug worldwide. It exhibits anti-inflammatory, anti-oxidative, anti-tumor, and anti-diabetic bioactivities; but its activity on diabetic-associated endothelial dysfunction is unknown. This study aimed to investigate the effect of purslane on endothelial function and the [...] Read more.
Portulaca oleracea L. (purslane) is a food and a traditional drug worldwide. It exhibits anti-inflammatory, anti-oxidative, anti-tumor, and anti-diabetic bioactivities; but its activity on diabetic-associated endothelial dysfunction is unknown. This study aimed to investigate the effect of purslane on endothelial function and the underlying mechanisms. Male C57BL/6 mice had 14-week ad libitum access to a high-fat rodent diet containing 60% kcal% fat to induce obesity and diabetes whereas purslane extract (200 mg/kg/day) was administered during the last 4 weeks via intragastric gavage. Primary rat aortic endothelial cells and isolated mouse aortas were cultured with a risk factor, high glucose or tunicamycin, together with purslane extract. By ESI-QTOF-MS/MS, flavonoids and their glycoside products were identified in the purslane extract. Exposure to high glucose or tunicamycin impaired acetylcholine-induced endothelium-dependent relaxations in aortas and induced endoplasmic reticulum (ER) stress and oxidative stress with the downregulation of 5′ AMP-activated protein kinase (AMPK)/ endothelial nitric oxide synthase (eNOS) signaling. Co-incubation with purslane significantly ameliorated these impairments. The effects of purslane were abolished by Compound C (AMPK inhibitor). Four-week purslane treatment ameliorated aortic relaxations, ER stress, and oxidative stress in diabetic obese mice. This study supported that purslane protected endothelial function, and inhibited ER stress and oxidative stress in vasculature through AMPK/eNOS activation, revealing its therapeutic potential against vascular complications in diabetes. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome and Cardiovascular Diseases)
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16 pages, 2673 KiB  
Article
AMPK-Dependent YAP Inhibition Mediates the Protective Effect of Metformin against Obesity-Associated Endothelial Dysfunction and Inflammation
by Lijing Kang, Juanjuan Yi, Chi-Wai Lau, Lei He, Qinghua Chen, Suowen Xu, Jun Li, Yin Xia, Yuanting Zhang, Yu Huang and Li Wang
Antioxidants 2023, 12(9), 1681; https://doi.org/10.3390/antiox12091681 - 28 Aug 2023
Cited by 4 | Viewed by 2228
Abstract
Hyperglycemia is a crucial risk factor for cardiovascular diseases. Chronic inflammation is a central characteristic of obesity, leading to many of its complications. Recent studies have shown that high glucose activates Yes-associated protein 1 (YAP) by suppressing AMPK activity in breast cancer cells. [...] Read more.
Hyperglycemia is a crucial risk factor for cardiovascular diseases. Chronic inflammation is a central characteristic of obesity, leading to many of its complications. Recent studies have shown that high glucose activates Yes-associated protein 1 (YAP) by suppressing AMPK activity in breast cancer cells. Metformin is a commonly prescribed anti-diabetic drug best known for its AMPK-activating effect. However, the role of YAP in the vasoprotective effect of metformin in diabetic endothelial cell dysfunction is still unknown. The present study aimed to investigate whether YAP activation plays a role in obesity-associated endothelial dysfunction and inflammation and examine whether the vasoprotective effect of metformin is related to YAP inhibition. Reanalysis of the clinical sequencing data revealed YAP signaling, and the YAP target genes CTGF and CYR61 were upregulated in aortic endothelial cells and retinal fibrovascular membranes from diabetic patients. YAP overexpression impaired endothelium-dependent relaxations (EDRs) in isolated mouse aortas and increased the expression of YAP target genes and inflammatory markers in human umbilical vein endothelial cells (HUVECs). High glucose-activated YAP in HUVECs and aortas was accompanied by increased production of oxygen-reactive species. AMPK inhibition was found to induce YAP activation, resulting in increased JNK activity. Metformin activated AMPK and promoted YAP phosphorylation, ultimately improving EDRs and suppressing the JNK activity. Targeting the AMPK–YAP–JNK axis could become a therapeutic strategy for alleviating vascular dysfunction in obesity and diabetes. Full article
(This article belongs to the Special Issue Oxidative Stress in Metabolic Syndrome and Cardiovascular Diseases)
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