Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.5
5.2
Journals
Cells
Special Issues
The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition
share announcement

The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition

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

Deadline for manuscript submissions: 15 June 2026 | Viewed by 6383

Special Issue Editors

Dr. Liya Yin

E-Mail Website
Guest Editor
College of Medicine, University of Arizona, Phoenix, AZ 85004, USA
Interests: lipid metabolism and atherosclerosis; angiogenesis, arteriogenesis and coronary collateral growth; microcirculation and cardiac blood flow regulation; cell reprogramming and stem cells in cardiovascular regeneration; microvascular dysfunction and diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Chuanxi Cai

E-Mail Website
Guest Editor
Department of Surgery, University of Virginia School of Medicine, Charlottesville, VA 22903, USA
Interests: cell survival; apoptosis; cell proliferation; senescence; progenitor cells; cancer; heart failure; long noncoding RNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. The production of reactive oxygen species (ROS) in the heart and blood vessels plays an essential role in maintaining the homeostasis of the cardiovascular system. However, ROS production is a double-edged sword. Transient and low-level ROS production within the cardiovascular system triggers cell signaling pathways that lead to hormetic adaptation. In contrast, the continuous production or accumulation of high levels of ROS results in pathological injury in the cardiomyocytes and vascular cells.

Oxidative stress occurs when the overproduction of ROS overwhelms the elimination ability of antioxidants. Accumulating evidence has shown that oxidative stress plays a critical role in the development and progression of CVD and has also been associated with mitochondrial dysfunction and chronic inflammation in the cardiovascular system. Cardiovascular risk factors include dietary habits, physical activity, smoking, metabolic syndromes, hypertension, high lipid levels, and chronic inflammation, all of which are related to oxidative stress and the overall impact of CVD incidence and outcome. Targeting the underlying molecular mechanism to regulate ROS production and oxidative stress may enable the development of novel and effective therapeutic strategies against various cardiovascular disorders. However, it is still an enigma as to how the comprehensive oxidative stress-related signaling pathways are orchestrated in cardiovascular physiology and pathology contexts.

This Special Issue of Cells aims to address the complexity of ROS signaling in CVD, to update our knowledge on the regulation of oxidative stress in cardiovascular disorders, and to identify potential clinical therapeutical targets. We welcome original research and review articles on state-of-the-art technologies and the latest findings in the field. Moreover, this Special Issue will cover broad aspects of these critical scientific areas, from in vitro cellular studies to the in vivo physiological and pathological aspects of oxidative stress in the cardiovascular system.

Dr. Liya Yin
Dr. Chuanxi Cai
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 250 words) can be sent to the Editorial Office for assessment.

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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
  • antioxidants
  • apoptosis
  • atherosclerosis
  • blood vessel
  • heart failure
  • hypertension
  • inflammation
  • mitochondria
  • microcirculation
  • reactive oxygen species

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

19 pages, 3768 KB  
Article
CISAT, a CoPP-Induced lncRNA, Improves Cardiac Mesenchymal Progenitor Cell Survival and Myocardial Repair via SFPQ/NRF2/p38 Redox Regulation
by Xiuchun Li, Xiao-Liang Wang, Sofia Lopez, Jill Wang and Chuanxi Cai
Cells 2026, 15(6), 557; https://doi.org/10.3390/cells15060557 - 20 Mar 2026
Viewed by 485
Abstract
Cellular therapy using human cardiac mesenchymal progenitor cells (hMPCs) for regenerative medicine is hindered by poor cell survival and senescence. Long non-coding RNAs (lncRNAs) are critical regulators of cellular processes, yet their role in cardiac aging remains underexplored. Here, lncRNA microarray profiling identified [...] Read more.
Cellular therapy using human cardiac mesenchymal progenitor cells (hMPCs) for regenerative medicine is hindered by poor cell survival and senescence. Long non-coding RNAs (lncRNAs) are critical regulators of cellular processes, yet their role in cardiac aging remains underexplored. Here, lncRNA microarray profiling identified a novel lncRNA, XLOC_002543, upregulated in hMPCs preconditioned with cobalt protoporphyrin (CoPP), which was named CoPP-Induced and SFPQ-Associated RNA Transcript (CISAT) due to its interaction with splicing factor proline and glutamine rich (SFPQ), confirmed via RNA pull-down and immunoprecipitation. CISAT was the only highly expressed transcript among seven lnc-ANKMY1-5 variants in hMPCs, as shown by RT-PCR. Notably, CISAT expression decreased in aging/senescent hMPCs, correlating with elevated p16INK4A, a senescence marker. Overexpression of CISAT reduced p16INK4A levels; enhanced hMPC survival, proliferation, and migration; and increased antioxidant and anti-apoptotic protein expression, while CISAT knockdown reduced resistance to H2O2-induced oxidative stress. In vivo, intramyocardial transplantation of CISAT-overexpressed hMPCs in an immune-deficient murine myocardial infarction model reduced fibrosis, promoted angiogenesis, and preserved cardiac function. Mechanistically, CISAT interacts with SFPQ to regulate NRF2-mediated redox homeostasis and inhibits p38 MAPK phosphorylation, mitigating senescence and enhancing cell survival. These findings suggest that targeting CISAT to modulate redox signaling and p38 MAPK pathways in aging hMPCs could improve their therapeutic efficacy for myocardial repair in heart disease. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition)
►▼ Show Figures

Graphical abstract

15 pages, 1293 KB  
Article
Preventive Aerobic Training Protects Against Doxorubicin-Induced Cardiotoxicity by Preserving Redox Status and Attenuating Cardiac Stress-Related Signaling
by Paola Victória da Costa Ghignatti, Rafael Aguiar Marschner, Rafael Teixeira Ribeiro, Vitor Gayger-Dias, Vanessa-Fernanda Da Silva, Luciele Varaschini Teixeira, Simone Wajner, Maximiliano Isoppo Schaun, Carlos-Alberto Gonçalves and Patrícia Sesterheim
Cells 2026, 15(5), 408; https://doi.org/10.3390/cells15050408 - 26 Feb 2026
Viewed by 677
Abstract
Doxorubicin (DOX) is a highly effective chemotherapeutic agent whose clinical use is limited by dose-dependent cardiotoxicity associated with oxidative stress, inflammation, and cellular stress responses. Here, we investigated whether preventive aerobic training could protect against DOX-induced cardiac injury in Wistar rats. Animals were [...] Read more.
Doxorubicin (DOX) is a highly effective chemotherapeutic agent whose clinical use is limited by dose-dependent cardiotoxicity associated with oxidative stress, inflammation, and cellular stress responses. Here, we investigated whether preventive aerobic training could protect against DOX-induced cardiac injury in Wistar rats. Animals were assigned to sedentary control (C), sedentary DOX (D), trained control (CT), and trained DOX (DT) groups. The moderate-intensity (~50–80% maximal exercise test) treadmill protocol (40 min/day, 4 days/week for 4 weeks) was performed before intraperitoneal administration of DOX (4 mg/kg, weekly for 4 weeks) or saline. Preventive training markedly improved exercise capacity (p < 0.001) and attenuated oxidative damage, maintaining antioxidant enzyme activity (GR, SOD) at control levels (p > 0.05). DOX significantly upregulated cardiac IL-6 and IL-1β expression (p < 0.01), while trained animals preserved IL-1β expression similar to controls (p > 0.99). In parallel, DOX increased cardiac HIF-1 expression (p < 0.05), indicating activation of hypoxia- and stress-related signaling pathways, an effect that was attenuated by preventive training (p > 0.99). DOX-induced cardiac atrophy was evidenced by reduced left ventricular mass (p < 0.001), which was partially prevented by training (p < 0.05). Although hematological toxicity persisted, preventive aerobic exercise effectively counteracted DOX cardiotoxicity by restoring redox homeostasis, dampening inflammation, and limiting apoptotic signaling. Collectively, these findings highlight exercise preconditioning as a promising non-pharmacological strategy in cardio-oncology to mitigate chemotherapy-associated cardiac injury. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition)
►▼ Show Figures

Figure 1

19 pages, 2894 KB  
Article
Inhibition of the JAK and MEK Pathways Limits Mitochondrial ROS Production in Human Saphenous Vein Smooth Muscle Cells
by Israel O. Bolanle, James P. Hobkirk, Mahmoud Loubani, Roger G. Sturmey and Timothy M. Palmer
Cells 2026, 15(2), 159; https://doi.org/10.3390/cells15020159 - 15 Jan 2026
Viewed by 635
Abstract
Activation of JAK/STAT and MAPK/ERK1,2 signalling pathways has been shown to increase the production of reactive oxygen species (ROS) in multiple cell types involved in cardiovascular diseases (CVDs), including vascular smooth muscle cells (VSMCs). However, these have not yet been studied in human [...] Read more.
Activation of JAK/STAT and MAPK/ERK1,2 signalling pathways has been shown to increase the production of reactive oxygen species (ROS) in multiple cell types involved in cardiovascular diseases (CVDs), including vascular smooth muscle cells (VSMCs). However, these have not yet been studied in human saphenous vein SMCs (HSVSMCs) responsible for the maladaptive remodelling leading to saphenous vein graft failure (VGF), to which patients with type 2 diabetes mellitus (T2DM) are more susceptible. Therefore, this study aimed to evaluate the contributions of the JAK/STAT and MAPK/ERK1,2 pathways towards production of mitochondrial ROS (mROS) in HSVSMCs from T2DM patients versus non-diabetic controls. HSVSMCs explanted from surplus HSV tissues from consenting patients undergoing coronary artery bypass graft surgery were stimulated in vitro with mitogenic stimuli known to be involved in neointimal hyperplasia (NIH) and VGF, which are known activators of the JAK/STAT and the MAPK/ERK1,2 signalling pathways. Flow cytometry was then used to analyse the production of mROS (superoxide) in MitoSOX-stained HSVSMCs. Additionally, we examined the effect of ruxolitinib and trametinib, selective inhibitors of JAK1/2 and MEK1/2 signalling pathways, respectively, on mROS levels in these cells. From our findings, mROS production was significantly higher in HSVSMCs from T2DM patients versus non-diabetic controls. Activation of either the JAK/STAT or MAPK/ERK1,2 signalling pathways did not significantly alter the production of mROS in HSVSMCs from both T2DM and non-diabetic patients. However, inhibition of JAK/STAT and MAPK/ERK1,2 signalling pathways with ruxolitinib and trametinib, respectively, resulted in a significant reduction in mROS in HSVSMCs from both T2DM and non-diabetic patients. Our findings demonstrate a JAK/STAT- and MAPK/ERK1,2-mediated production of mROS in HSVSMCs. Hence, they are potential targets for drug development to limit ROS production in ROS-driven proliferation and migration of HSVSMCs responsible for VGF. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition)
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

15 pages, 1127 KB  
Review
Cardiac Aging in the Multi-Omics Era: High-Throughput Sequencing Insights
by Yiran Song, Brian Spurlock, Jiandong Liu and Li Qian
Cells 2024, 13(20), 1683; https://doi.org/10.3390/cells13201683 - 11 Oct 2024
Cited by 3 | Viewed by 3713
Abstract
Cardiovascular diseases are a leading cause of mortality worldwide, and the risks of both developing a disease and receiving a poor prognosis increase with age. With increasing life expectancy, understanding the mechanisms underlying heart aging has become critical. Traditional techniques have supported research [...] Read more.
Cardiovascular diseases are a leading cause of mortality worldwide, and the risks of both developing a disease and receiving a poor prognosis increase with age. With increasing life expectancy, understanding the mechanisms underlying heart aging has become critical. Traditional techniques have supported research into finding the physiological changes and hallmarks of cardiovascular aging, including oxidative stress, disabled macroautophagy, loss of proteostasis, and epigenetic alterations, among others. The advent of high-throughput multi-omics techniques offers new perspectives on the molecular mechanisms and cellular processes in the heart, guiding the development of therapeutic targets. This review explores the contributions and characteristics of these high-throughput techniques to unraveling heart aging. We discuss how different high-throughput omics approaches, both alone and in combination, produce robust and exciting new findings and outline future directions and prospects in studying heart aging in this new era. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases—2nd Edition)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop