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Redox Regulation of Cardiovascular Metabolism and Inflammation
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Redox Regulation of Cardiovascular Metabolism and Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 24670

Special Issue Editors

Prof. Dr. Francis J. Miller, Jr.

E-Mail Website
Guest Editor
Department of Internal Medicine, Duke University, Durham, NC, USA
Interests: atherosclerosis; reactive oxygen species; oxidative stress; smooth muscle cells; NADPH oxidases; restenosis; redox signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Siobhan M. Craige

E-Mail Website
Guest Editor
Department of Human Nutrition, Foods, and Exercise, Virginia Tech University, Blacksburg, VA, USA
Interests: redox signaling; reactive oxygen species; endothelial cells; NADPH oxidases; cardiometabolic disease; exercise; diet

Special Issue Information

Dear Colleagues,

In the last three decades, advances in research and therapeutics have signicantly reduced the morbidity and mortality associated with cardiovascular-related diseases. However, as obesity and metabolic syndrome are rapidly becoming a world-wide epidemic, the incidence of cardiovascular disase is on the rise and there is a critical need for new molecular targets that take into account these co-morbidities. Reactive oxygen species (ROS) production is an integral part of both normal cardiometabolic homeostasis and cardiometabolic pathologies. The dual role of ROS is underscored by the failure of antioxidant therapies to provide clear cardiometabolic benefits. Furthermore, the adaptive responses of the vasculature to exercise, which protect from cardiometabolic diseases, are dependent on ROS signaling. Indeed, recent studies have demonstrated that ROS are necessary for the regulation of a myriad of normal cellular redox processes, including intracellular signaling, metabolic homeostasis, and transcriptional regulation. In terms of pathology, most cardiometabolic diseases demonstrate signatures of ROS damage and chronic inflammation. ROS are both mediators of pro-inflammatory signaling and the product of inflammation, and likely contribute to a toxic milieu that furthers tissue damage in disease states. In fact, a recent clinical trial demonstrated the effectiveness of targeting inflammation by reducing injury during major cardiovascular events. Therefore, understanding the intersection between inflammation, reactive oxygen species, metabolism, and exercise adaptation in physiologic and pathologic settings is essential to a better understanding of cardiometabolic health, disease, and thereapeutic strategies.

The goal of this special issue is to assemble a collection of state-of-the-art research and review articles describing:

  1. Mechanisms of ROS regulation including timing, location, and sources of obesity (e.g., NADPH oxidases, nitric oxide synthase, lipoxygenases, mitochondria), and inflammation and metabolic syndrome in the context of cardiovascular disease.
  2. Pharmacologic and non-pharmacologic strategies of manipulating localized redox-signaling pathways to prevent cardiovascular consequences, including inflammation and dysregulation of cardiovascular metabolism.
  3. Redox mechanisms by which diet and/or exercise modify inflammation and the effects of cardiovascular diseases and cardiometabolic syndrome.

Prof. Dr. Francis J. Miller, Jr.
Dr. Siobhan M. Craige
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • Redox signaling: oxidative stress, reactive oxygen species, NADPH oxidase, mitochondria, antioxidants
  • Inflammation: cytokines, chemokines, inflammatory signaling
  • Cardiometabolic diseases: diabetes, obesity, metabolism, metabolic disease
  • Exercise: exercise adaptation, cardiometabolic preconditioning, exercise to prevent disease
  • Heart disease: myocardial infarction, ischemia/reperfusion, cardiometabolic dysfunction
  • Vascular disease: atherosclerosis, hypertension, restenosis, stroke, neointima, thrombosis, peripheral artery disease, aneurysm, vasculitis

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Published Papers (5 papers)

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Research

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20 pages, 5925 KiB  
Article
Redox Signaling and Regional Heterogeneity of Endothelial Dysfunction in db/db Mice
by Nada A. Sallam and Ismail Laher
Int. J. Mol. Sci. 2020, 21(17), 6147; https://doi.org/10.3390/ijms21176147 - 26 Aug 2020
Cited by 8 | Viewed by 3033
Abstract
The variable nature of vascular dysfunction in diabetes is not well understood. We explored the functional adaptation of different arteries in db/db mice in relation to increased severity and duration of diabetes. We compared endothelium-dependent and -independent vasodilation in the aortae, as well [...] Read more.
The variable nature of vascular dysfunction in diabetes is not well understood. We explored the functional adaptation of different arteries in db/db mice in relation to increased severity and duration of diabetes. We compared endothelium-dependent and -independent vasodilation in the aortae, as well as the carotid and femoral arteries, of db/db mice at three ages in parallel with increased body weight, oxidative stress, and deterioration of glycemic control. Vascular responses to in vitro generation of reactive oxygen species (ROS) and expression of superoxide dismutase (SOD) isoforms were assessed. There was a progressive impairment of endothelium-dependent and -independent vasorelaxation in the aortae of db/db mice. The carotid artery was resistant to the effects of in vivo and in vitro induced oxidative stress, and it maintained unaltered vasodilatory responses, likely because the carotid artery relaxed in response to ROS. The femoral artery was more reliant on dilation mediated by endothelium-dependent hyperpolarizing factor(s), which was reduced in db/db mice at the earliest age examined and did not deteriorate with age. Substantial heterogeneity exists between the three arteries in signaling pathways and protein expression of SODs under physiological and diabetic conditions. A better understanding of vascular heterogeneity will help develop novel therapeutic approaches for targeted vascular treatments, including blood vessel replacement. Full article
(This article belongs to the Special Issue Redox Regulation of Cardiovascular Metabolism and Inflammation)
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16 pages, 3936 KiB  
Article
Systems Approach to Study Associations between OxLDL and Abdominal Aortic Aneurysms
by Łukasz Gutowski, Kaja Gutowska, Maria Pioruńska-Stolzmann, Piotr Formanowicz and Dorota Formanowicz
Int. J. Mol. Sci. 2019, 20(16), 3909; https://doi.org/10.3390/ijms20163909 - 11 Aug 2019
Cited by 9 | Viewed by 3924
Abstract
Although abdominal aortic aneurysm (AAA) is a common vascular disease and is associated with high mortality, the full pathogenesis of AAA remains unknown to researchers. Abdominal aortic aneurysms and atherosclerosis are strongly related. Currently, it is more often suggested that development of AAA [...] Read more.
Although abdominal aortic aneurysm (AAA) is a common vascular disease and is associated with high mortality, the full pathogenesis of AAA remains unknown to researchers. Abdominal aortic aneurysms and atherosclerosis are strongly related. Currently, it is more often suggested that development of AAA is not a result of atherosclerosis, however, individual factors can act independently or synergistically with atherosclerosis. One of such factors is low-density lipoprotein (LDL) and its oxidized form (oxLDL). It is known that oxLDL plays an important role in the pathogenesis of atherosclerosis, thus, we decided to examine oxLDL impact on the development of AAA by creating two models using Petri-nets. The first, full model, contains subprocess of LDL oxidation and all subprocesses in which it participates, while the second, reduced model, does not contain them. The analysis of such models can be based on t-invariants. They correspond to subprocesses which do not change the state of the modeled system. Moreover, the knockout analysis has been used to estimate how crucial a selected transition (representing elementary subprocess) is, based on the number of excluded subprocesses as a result of its knockout. The results of the analysis of our models show that oxLDL affects 55.84% of subprocesses related to AAA development, but the analysis of the nets based on knockouts and simulation has shown that the influence of oxLDL on enlargement and rupture of AAA is negligible. Full article
(This article belongs to the Special Issue Redox Regulation of Cardiovascular Metabolism and Inflammation)
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Review

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14 pages, 514 KiB  
Review
How Periodontal Disease and Presence of Nitric Oxide Reducing Oral Bacteria Can Affect Blood Pressure
by Pamela Pignatelli, Giulia Fabietti, Annalisa Ricci, Adriano Piattelli and Maria Cristina Curia
Int. J. Mol. Sci. 2020, 21(20), 7538; https://doi.org/10.3390/ijms21207538 - 13 Oct 2020
Cited by 55 | Viewed by 9963
Abstract
Nitric oxide (NO), a small gaseous and multifunctional signaling molecule, is involved in the maintenance of metabolic and cardiovascular homeostasis. It is endogenously produced in the vascular endothelium by specific enzymes known as NO synthases (NOSs). Subsequently, NO is readily oxidized to nitrite [...] Read more.
Nitric oxide (NO), a small gaseous and multifunctional signaling molecule, is involved in the maintenance of metabolic and cardiovascular homeostasis. It is endogenously produced in the vascular endothelium by specific enzymes known as NO synthases (NOSs). Subsequently, NO is readily oxidized to nitrite and nitrate. Nitrite is also derived from exogenous inorganic nitrate (NO3) contained in meat, vegetables, and drinking water, resulting in greater plasma NO2 concentration and major reduction in systemic blood pressure (BP). The recycling process of nitrate and nitrite to NO (nitrate-nitrite-NO pathway), known as the enterosalivary cycle of nitrate, is dependent upon oral commensal nitrate-reducing bacteria of the dorsal tongue. Veillonella, Actinomyces, Haemophilus, and Neisseria are the most copious among the nitrate-reducing bacteria. The use of chlorhexidine mouthwashes and tongue cleaning can mitigate the bacterial nitrate-related BP lowering effects. Imbalances in the oral reducing microbiota have been associated with a decrease of NO, promoting endothelial dysfunction, and increased cardiovascular risk. Although there is a relationship between periodontitis and hypertension (HT), the correlation between nitrate-reducing bacteria and HT has been poorly studied. Restoring the oral flora and NO activity by probiotics may be considered a potential therapeutic strategy to treat HT. Full article
(This article belongs to the Special Issue Redox Regulation of Cardiovascular Metabolism and Inflammation)
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14 pages, 1337 KiB  
Review
The Redox-Sensitive Na/K-ATPase Signaling in Uremic Cardiomyopathy
by Jiang Liu, Ying Nie, Muhammad Chaudhry, Fang Bai, Justin Chuang, Komal Sodhi and Joseph I. Shapiro
Int. J. Mol. Sci. 2020, 21(4), 1256; https://doi.org/10.3390/ijms21041256 - 13 Feb 2020
Cited by 18 | Viewed by 3934
Abstract
In recent years, Na/K-ATPase signaling has been implicated in different physiological and pathophysiological conditions, including cardiac hypertrophy and uremic cardiomyopathy. Cardiotonic steroids (CTS), specific ligands of Na/K-ATPase, regulate its enzymatic activity (at higher concentrations) and signaling function (at lower concentrations without significantly affecting [...] Read more.
In recent years, Na/K-ATPase signaling has been implicated in different physiological and pathophysiological conditions, including cardiac hypertrophy and uremic cardiomyopathy. Cardiotonic steroids (CTS), specific ligands of Na/K-ATPase, regulate its enzymatic activity (at higher concentrations) and signaling function (at lower concentrations without significantly affecting its enzymatic activity) and increase reactive oxygen species (ROS) generation. On the other hand, an increase in ROS alone also regulates the Na/K-ATPase enzymatic activity and signaling function. We termed this phenomenon the Na/K-ATPase-mediated oxidant-amplification loop, in which oxidative stress regulates both the Na/K-ATPase activity and signaling. Most recently, we also demonstrated that this amplification loop is involved in the development of uremic cardiomyopathy. This review aims to evaluate the redox-sensitive Na/K-ATPase-mediated oxidant amplification loop and uremic cardiomyopathy. Full article
(This article belongs to the Special Issue Redox Regulation of Cardiovascular Metabolism and Inflammation)
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16 pages, 1078 KiB  
Review
Mechanistic Insight of Na/K-ATPase Signaling and HO-1 into Models of Obesity and Nonalcoholic Steatohepatitis
by Rebecca Pratt, Hari Vishal Lakhani, Mishghan Zehra, Rutmann Desauguste, Sneha S. Pillai and Komal Sodhi
Int. J. Mol. Sci. 2020, 21(1), 87; https://doi.org/10.3390/ijms21010087 - 21 Dec 2019
Cited by 7 | Viewed by 3255
Abstract
Obesity is a multifaceted pathophysiological condition that has been associated with lipid accumulation, adipocyte dysfunction, impaired mitochondrial biogenesis and an altered metabolic profile. Redox imbalance and excessive release of inflammatory mediators have been intricately linked in obesity-associated phenotypes. Hence, understanding the mechanisms of [...] Read more.
Obesity is a multifaceted pathophysiological condition that has been associated with lipid accumulation, adipocyte dysfunction, impaired mitochondrial biogenesis and an altered metabolic profile. Redox imbalance and excessive release of inflammatory mediators have been intricately linked in obesity-associated phenotypes. Hence, understanding the mechanisms of redox signaling pathways and molecular targets exacerbating oxidative stress is crucial in improving health outcomes. The activation of Na/K-ATPase/Src signaling, and its downstream pathways, by reactive oxygen species (ROS) has been recently implicated in obesity and subsequent nonalcoholic steatohepatitis (NASH), which causes further production of ROS creating an oxidant amplification loop. Apart from that, numerous studies have also characterized antioxidant properties of heme oxygenase 1 (HO-1), which is suppressed in an obese state. The induction of HO-1 restores cellular redox processes, which contributes to inhibition of the toxic milieu. The novelty of these independent mechanisms presents a unique opportunity to unravel their potential as molecular targets for redox regulation in obesity and NASH. The attenuation of oxidative stress, by understanding the underlying molecular mechanisms and associated mediators, with a targeted treatment modality may provide for improved therapeutic options to combat clinical disorders. Full article
(This article belongs to the Special Issue Redox Regulation of Cardiovascular Metabolism and Inflammation)
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