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Cells
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The Role of Oxidative Stress in Cardiovascular Diseases
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The Role of Oxidative Stress in Cardiovascular Diseases

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

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 46127

Special Issue Editors

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
Dr. Liya Yin

E-Mail Website
Guest Editor
Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, 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

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) 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. Chuanxi Cai
Dr. Liya Yin
Guest Editors

Manuscript Submission Information

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Keywords

  • oxidative stress
  • antioxidants
  • apoptosis
  • atherosclerosis
  • blood vessel
  • heart failure
  • hypertension
  • inflammation
  • mitochondria
  • microcirculation
  • reactive oxygen species

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Related Special Issue

Published Papers (9 papers)

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Research

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17 pages, 2553 KiB  
Article
Overexpression of GREM1 Improves the Survival Capacity of Aged Cardiac Mesenchymal Progenitor Cells via Upregulation of the ERK/NRF2-Associated Antioxidant Signal Pathway
by Gurleen Kaur, Xiaoliang Wang, Xiuchun Li, Hannah Ong, Xiangfei He and Chuanxi Cai
Cells 2023, 12(8), 1203; https://doi.org/10.3390/cells12081203 - 21 Apr 2023
Cited by 1 | Viewed by 2646
Abstract
Ischemic heart disease is the leading cause of mortality in the United States. Progenitor cell therapy can restore myocardial structure and function. However, its efficacy is severely limited by cell aging and senescence. Gremlin-1 (GREM1), a member of the bone morphogenetic protein antagonist [...] Read more.
Ischemic heart disease is the leading cause of mortality in the United States. Progenitor cell therapy can restore myocardial structure and function. However, its efficacy is severely limited by cell aging and senescence. Gremlin-1 (GREM1), a member of the bone morphogenetic protein antagonist family, has been implicated in cell proliferation and survival. However, GREM1’s role in cell aging and senescence has never been investigated in human cardiac mesenchymal progenitor cells (hMPCs). Therefore, this study assessed the hypothesis that overexpression of GREM1 rejuvenates the cardiac regenerative potential of aging hMPCs to a youthful stage and therefore allows better capacity for myocardial repair. We recently reported that a subpopulation of hMPCs with low mitochondrial membrane potential can be sorted from right atrial appendage-derived cells in patients with cardiomyopathy and exhibit cardiac reparative capacity in a mouse model of myocardial infarction. In this study, lentiviral particles were used to overexpress GREM1 in these hMPCs. Protein and mRNA expression were assessed through Western blot and RT-qPCR. FACS analysis for Annexin V/PI staining and lactate dehydrogenase assay were used to assess cell survival. It was observed that cell aging and cell senescence led to a decrease in GREM1 expression. In addition, overexpression of GREM1 led to a decrease in expression of senescence genes. Overexpression of GREM1 led to no significant change in cell proliferation. However, GREM1 appeared to have an anti-apoptotic effect, with an increase in survival and decrease in cytotoxicity evident in GREM1-overexpressing hMPCs. Overexpressing GREM1 also induced cytoprotective properties by decreasing reactive oxidative species and mitochondrial membrane potential. This result was associated with increased expression of antioxidant proteins, such as SOD1 and catalase, and activation of the ERK/NRF2 survival signal pathway. Inhibition of ERK led to a decrease in GREM1-mediated rejuvenation in terms of cell survival, which suggests that an ERK-dependent pathway may be involved. Taken altogether, these results indicate that overexpression of GREM1 can allow aging hMPCs to adopt a more robust phenotype with improved survival capacity, which is associated with an activated ERK/NRF2 antioxidant signal pathway. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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21 pages, 5346 KiB  
Article
High Glucose Activates Prolyl Hydroxylases and Disrupts HIF-α Signaling via the P53/TIGAR Pathway in Cardiomyocyte
by Jian-Xiong Chen, Lanfang Li, Aubrey C. Cantrell, Quinesha A. Williams and Heng Zeng
Cells 2023, 12(7), 1060; https://doi.org/10.3390/cells12071060 - 31 Mar 2023
Viewed by 2209
Abstract
The induction of hypoxia tolerance has emerged as a novel therapeutic strategy for the treatment of ischemic diseases. The disruption of hypoxic signaling by hyperglycemia has been shown to contribute to diabetic cardiomyopathy. In this study, we explored the potential molecular mechanisms by [...] Read more.
The induction of hypoxia tolerance has emerged as a novel therapeutic strategy for the treatment of ischemic diseases. The disruption of hypoxic signaling by hyperglycemia has been shown to contribute to diabetic cardiomyopathy. In this study, we explored the potential molecular mechanisms by which high glucose (HG) impairs hypoxia-inducible factor-α (HIF-α) signaling in cardiomyocytes. The exposure of H9c2 cell lines to HG resulted in time- and concentration-dependent decreases in HIF-1α and HIF-2α expression together with an increase in prolyl hydroxylase-1,2 (PHD1 and PHD2) expression, the main regulators of HIF-α destabilization in the heart. The exposure of H9c2 cells to normal glucose (5.5 mM) and high glucose (15, 30, and 45 mM) led to dose-dependent increases in p53 and TIGAR and a decrease in SIRT3 expression. The pretreatment of H9c2 with p53 siRNA to knockdown p53 attenuated PHD1 and PHD2 expression, thus significantly enhancing HIF-1α and HIF-2α expression in H9c2 cells under HG conditions. Interestingly, pretreatment with p53 siRNA altered H9c2 cell metabolism by reducing oxygen consumption rate and increasing glycolysis. Similarly, pretreatment with TIGAR siRNA blunted HG-induced PHD1 and PHD2 expression. This was accompanied by an increase in HIF-1α and HIF-2α expression with a reduction in oxygen consumption rate in H9c2 cells. Furthermore, pretreatment with adenovirus-SIRT3 (Ad-SIRT3) significantly reduced the HG-induced expression of p53 and PHDs and increased HIF-1α levels in H9c2 cells. Ad-SIRT3 treatment also regulated PHDs-HIF-1α levels in the hearts of diabetic db/db mice. Our study revealed a novel role of the HG-induced disruption of PHDs-HIF-α signaling via upregulating p53 and TIGAR expression. Therefore, the p53/TIGAR signaling pathway may be a novel target for diabetic cardiomyopathy. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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17 pages, 8630 KiB  
Article
Spike Protein Impairs Mitochondrial Function in Human Cardiomyocytes: Mechanisms Underlying Cardiac Injury in COVID-19
by Tin Van Huynh, Lekha Rethi, Ting-Wei Lee, Satoshi Higa, Yu-Hsun Kao and Yi-Jen Chen
Cells 2023, 12(6), 877; https://doi.org/10.3390/cells12060877 - 11 Mar 2023
Cited by 13 | Viewed by 11732 | Correction
Abstract
Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key heart functions. We hypothesized that S1 would directly [...] Read more.
Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key heart functions. We hypothesized that S1 would directly impair the functions of cardiomyocyte mitochondria, thus causing cardiac dysfunction. Methods: Through the Seahorse Mito Stress Test and real-time ATP rate assays, we explored the mitochondrial bioenergetics in human cardiomyocytes (AC16). The cells were treated without (control) or with S1 (1 nM) for 24, 48, and 72 h and we observed the mitochondrial morphology using transmission electron microscopy and confocal fluorescence microscopy. Western blotting, XRhod-1, and MitoSOX Red staining were performed to evaluate the expression of proteins related to energetic metabolism and relevant signaling cascades, mitochondrial Ca2+ levels, and ROS production. Results: The 24 h S1 treatment increased ATP production and mitochondrial respiration by increasing the expression of fatty-acid-transporting regulators and inducing more negative mitochondrial membrane potential (Δψm). The 72 h S1 treatment decreased mitochondrial respiration rates and Δψm, but increased levels of reactive oxygen species (ROS), mCa2+, and intracellular Ca2+. Electron microscopy revealed increased mitochondrial fragmentation/fission in AC16 cells treated for 72 h. The effects of S1 on ATP production were completely blocked by neutralizing ACE2 but not CD147 antibodies, and were partly attenuated by Mitotempo (1 µM). Conclusion: S1 might impair mitochondrial function in human cardiomyocytes by altering Δψm, mCa2+ overload, ROS accumulation, and mitochondrial dynamics via ACE2. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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16 pages, 1921 KiB  
Article
Electrical Stimulation Increases the Secretion of Cardioprotective Extracellular Vesicles from Cardiac Mesenchymal Stem Cells
by Haitao Zhang, Yan Shen, Il-man Kim, Yutao Liu, Jingwen Cai, Adam E. Berman, Kent R. Nilsson, Neal L. Weintraub and Yaoliang Tang
Cells 2023, 12(6), 875; https://doi.org/10.3390/cells12060875 - 11 Mar 2023
Cited by 5 | Viewed by 2467
Abstract
Clinical trials have shown that electric stimulation (ELSM) using either cardiac resynchronization therapy (CRT) or cardiac contractility modulation (CCM) approaches is an effective treatment for patients with moderate to severe heart failure, but the mechanisms are incompletely understood. Extracellular vesicles (EV) produced by [...] Read more.
Clinical trials have shown that electric stimulation (ELSM) using either cardiac resynchronization therapy (CRT) or cardiac contractility modulation (CCM) approaches is an effective treatment for patients with moderate to severe heart failure, but the mechanisms are incompletely understood. Extracellular vesicles (EV) produced by cardiac mesenchymal stem cells (C-MSC) have been reported to be cardioprotective through cell-to-cell communication. In this study, we investigated the effects of ELSM stimulation on EV secretion from C-MSCs (C-MSCELSM). We observed enhanced EV-dependent cardioprotection conferred by conditioned medium (CM) from C-MSCELSM compared to that from non-stimulated control C-MSC (C-MSCCtrl). To investigate the mechanisms of ELSM-stimulated EV secretion, we examined the protein levels of neutral sphingomyelinase 2 (nSMase2), a key enzyme of the endosomal sorting complex required for EV biosynthesis. We detected a time-dependent increase in nSMase2 protein levels in C-MSCELSM compared to C-MSCCtrl. Knockdown of nSMase2 in C-MSC by siRNA significantly reduced EV secretion in C-MSCELSM and attenuated the cardioprotective effect of CM from C-MSCELSM in HL-1 cells. Taken together, our results suggest that ELSM-mediated increases in EV secretion from C-MSC enhance the cardioprotective effects of C-MSC through an EV-dependent mechanism involving nSMase2. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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16 pages, 331 KiB  
Article
Relationship between Oxidative Stress and Left Ventricle Markers in Patients with Chronic Heart Failure
by Aušra Mongirdienė, Agnė Liuizė, Dovilė Karčiauskaitė, Eglė Mazgelytė, Arūnas Liekis and Ilona Sadauskienė
Cells 2023, 12(5), 803; https://doi.org/10.3390/cells12050803 - 4 Mar 2023
Cited by 7 | Viewed by 1956
Abstract
Oxidative stress is proposed in the literature as an important player in the development of CHF and correlates with left ventricle (LV) dysfunction and hypertrophy in the failing heart. In this study, we aimed to verify if the serum oxidative stress markers differ [...] Read more.
Oxidative stress is proposed in the literature as an important player in the development of CHF and correlates with left ventricle (LV) dysfunction and hypertrophy in the failing heart. In this study, we aimed to verify if the serum oxidative stress markers differ in chronic heart failure (CHF) patients’ groups depending on the LV geometry and function. Patients were stratified into two groups according to left ventricular ejection fraction (LVEF) values: HFrEF (<40% (n = 27)) and HFpEF (≥40% (n = 33)). Additionally, patients were stratified into four groups according to LV geometry: NG–normal left ventricle geometry (n = 7), CR–concentric remodeling (n = 14), cLVH–concentric LV hypertrophy (n = 16), and eLVF–eccentric LV hypertrophy (n = 23). We measured protein (protein carbonyl (PC), nitrotyrosine (NT-Tyr), dityrosine), lipid (malondialdehyde (MDA), oxidizes (HDL) oxidation and antioxidant (catalase activity, total plasma antioxidant capacity (TAC) markers in serum. Transthoracic echocardiogram analysis and lipidogram were also performed. We found that oxidative (NT-Tyr, dityrosine, PC, MDA, oxHDL) and antioxidative (TAC, catalase) stress marker levels did not differ between the groups according to LVEF or LV geometry. NT-Tyr correlated with PC (rs = 0.482, p = 0.000098), and oxHDL (rs = 0.278, p = 0.0314). MDA correlated with total (rs = 0.337, p = 0.008), LDL (rs = 0.295, p = 0.022) and non-HDL (rs = 0.301, p = 0.019) cholesterol. NT-Tyr negatively correlated with HDL cholesterol (rs = -0.285, p = 0.027). LV parameters did not correlate with oxidative/antioxidative stress markers. Significant negative correlations were found between the end-diastolic volume of the LV and the end-systolic volume of the LV and HDL-cholesterol (rs = –0.935, p < 0.0001; rs = –0.906, p < 0.0001, respectively). Significant positive correlations between both the thickness of the interventricular septum and the thickness of the LV wall and the levels of triacylglycerol in serum (rs = 0.346, p = 0.007; rs = 0.329, p = 0.010, respectively) were found. In conclusions, we did not find a difference in serum concentrations of both oxidant (NT-Tyr, PC, MDA) and antioxidant (TAC and catalase) concentrations in CHF patients’ groups according to LV function and geometry was found. The geometry of the LV could be related to lipid metabolism in CHF patients, and no correlation between oxidative/antioxidant and LV markers in CHF patients was found. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
13 pages, 7579 KiB  
Article
The Roles of Bone Marrow-Derived Stem Cells in Coronary Collateral Growth Induced by Repetitive Ischemia
by Molly Enrick, Anurag Jamaiyar, Vahagn Ohanyan, Cody Juguilon, Christopher Kolz, Xin Shi, Danielle Janota, Weiguo Wan, Devan Richardson, Kelly Stevanov, Tatevik Hakobyan, Lindsay Shockling, Arianna Diaz, Sharon Usip, Feng Dong, Ping Zhang, William M. Chilian and Liya Yin
Cells 2023, 12(2), 242; https://doi.org/10.3390/cells12020242 - 6 Jan 2023
Cited by 2 | Viewed by 1942
Abstract
Many clinical trials have attempted to use stem cells to treat ischemic heart diseases (IHD), but the benefits have been modest. Though coronary collaterals can be a “natural bypass” for IHD patients, the regulation of coronary collateral growth (CCG) and the role of [...] Read more.
Many clinical trials have attempted to use stem cells to treat ischemic heart diseases (IHD), but the benefits have been modest. Though coronary collaterals can be a “natural bypass” for IHD patients, the regulation of coronary collateral growth (CCG) and the role of endogenous stem cells in CCG are not fully understood. In this study, we used a bone marrow transplantation scheme to study the role of bone marrow stem cells (BMSCs) in a rat model of CCG. Transgenic GFP rats were used to trace BMSCs after transplantation; GFP bone marrow was harvested or sorted for bone marrow transplantation. After recovering from transplantation, the recipient rats underwent 10 days of repetitive ischemia (RI), with echocardiography before and after RI, to measure cardiac function and myocardial blood flow. At the end of RI, the rats were sacrificed for the collection of bone marrow for flow cytometry or heart tissue for imaging analysis. Our study shows that upon RI stimulation, BMSCs homed to the recipient rat hearts’ collateral-dependent zone (CZ), proliferated, differentiated into endothelial cells, and engrafted in the vascular wall for collateral growth. These RI-induced collaterals improved coronary blood flow and cardiac function in the recipients’ hearts during ischemia. Depletion of donor CD34+ BMSCs led to impaired CCG in the recipient rats, indicating that this cell population is essential to the process. Overall, these results show that BMSCs contribute to CCG and suggest that regulation of the function of BMSCs to promote CCG might be a potential therapeutic approach for IHD. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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Review

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24 pages, 2569 KiB  
Review
Oxidative Stress and MicroRNAs in Endothelial Cells under Metabolic Disorders
by Morgan Minjares, Wendy Wu and Jie-Mei Wang
Cells 2023, 12(9), 1341; https://doi.org/10.3390/cells12091341 - 8 May 2023
Cited by 13 | Viewed by 3945
Abstract
Reactive oxygen species (ROS) are radical oxygen intermediates that serve as important second messengers in signal transduction. However, when the accumulation of these molecules exceeds the buffering capacity of antioxidant enzymes, oxidative stress and endothelial cell (EC) dysfunction occur. EC dysfunction shifts the [...] Read more.
Reactive oxygen species (ROS) are radical oxygen intermediates that serve as important second messengers in signal transduction. However, when the accumulation of these molecules exceeds the buffering capacity of antioxidant enzymes, oxidative stress and endothelial cell (EC) dysfunction occur. EC dysfunction shifts the vascular system into a pro-coagulative, proinflammatory state, thereby increasing the risk of developing cardiovascular (CV) diseases and metabolic disorders. Studies have turned to the investigation of microRNA treatment for CV risk factors, as these post-transcription regulators are known to co-regulate ROS. In this review, we will discuss ROS pathways and generation, normal endothelial cell physiology and ROS-induced dysfunction, and the current knowledge of common metabolic disorders and their connection to oxidative stress. Therapeutic strategies based on microRNAs in response to oxidative stress and microRNA’s regulatory roles in controlling ROS will also be explored. It is important to gain an in-depth comprehension of the mechanisms generating ROS and how manipulating these enzymatic byproducts can protect endothelial cell function from oxidative stress and prevent the development of vascular disorders. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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20 pages, 1517 KiB  
Review
The Role of Oxidative Stress in Atherosclerosis
by Matthew Batty, Martin R. Bennett and Emma Yu
Cells 2022, 11(23), 3843; https://doi.org/10.3390/cells11233843 - 30 Nov 2022
Cited by 129 | Viewed by 14546
Abstract
Atherosclerosis is a chronic inflammatory disease of the vascular system and is the leading cause of cardiovascular diseases worldwide. Excessive generation of reactive oxygen species (ROS) leads to a state of oxidative stress which is a major risk factor for the development and [...] Read more.
Atherosclerosis is a chronic inflammatory disease of the vascular system and is the leading cause of cardiovascular diseases worldwide. Excessive generation of reactive oxygen species (ROS) leads to a state of oxidative stress which is a major risk factor for the development and progression of atherosclerosis. ROS are important for maintaining vascular health through their potent signalling properties. However, ROS also activate pro-atherogenic processes such as inflammation, endothelial dysfunction and altered lipid metabolism. As such, considerable efforts have been made to identify and characterise sources of oxidative stress in blood vessels. Major enzymatic sources of vascular ROS include NADPH oxidases, xanthine oxidase, nitric oxide synthases and mitochondrial electron transport chains. The production of ROS is balanced by ROS-scavenging antioxidant systems which may become dysfunctional in disease, contributing to oxidative stress. Changes in the expression and function of ROS sources and antioxidants have been observed in human atherosclerosis while in vitro and in vivo animal models have provided mechanistic insight into their functions. There is considerable interest in utilising antioxidant molecules to balance vascular oxidative stress, yet clinical trials are yet to demonstrate any atheroprotective effects of these molecules. Here we will review the contribution of ROS and oxidative stress to atherosclerosis and will discuss potential strategies to ameliorate these aspects of the disease. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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22 pages, 946 KiB  
Review
Contribution of Oxidative Stress (OS) in Calcific Aortic Valve Disease (CAVD): From Pathophysiology to Therapeutic Targets
by Daniela Maria Tanase, Emilia Valasciuc, Evelina Maria Gosav, Mariana Floria, Claudia Florida Costea, Nicoleta Dima, Ionut Tudorancea, Minela Aida Maranduca and Ionela Lacramioara Serban
Cells 2022, 11(17), 2663; https://doi.org/10.3390/cells11172663 - 27 Aug 2022
Cited by 13 | Viewed by 3740
Abstract
Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative [...] Read more.
Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Cardiovascular Diseases)
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