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Antioxidants
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Protective Effects of H2S and H2S-Releasing...
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Protective Effects of H2S and H2S-Releasing Drugs in 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: closed (15 April 2021) | Viewed by 28737

Special Issue Editors

Dr. Lara Testai

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, Via Bonanno Pisano 6, 56126 Pisa, Italy
Interests: hydrogen sulfide (H2S); cardiovascular system; ageing; potassium channels; mitochondria
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Vincenzo Calderone

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, Via Bonanno Pisano 6, 56126 Pisa, Italy
Interests: H2S; gasotransmitters; cardiovascular pharmacology; ion channels; metabolic pharmacology; synthetic and natural H2S donors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hydrogen sulfide (H2S), originally known for its toxic and malodorous properties, is now recognized as a gaseous mediator endowed with beneficial effects for humans. Indeed, an increasing body of evidence suggests the involvement of H2S in different physiological and pathological processes, including those of the cardiovascular system. It is well-known that cardiovascular diseases are the main cause of morbidity and mortality in Western countries, and several risk factors contribute to their development and progression. Metabolic disorders such as metabolic syndrome and diabetes, lifestyle, and ageing may favor the onset of cardiovascular diseases. In this context H2S is a key player able to elicit protective actions through several mechanisms, such as antioxidative and anti-inflammatory action, preservation of mitochondrial function, reduction of apoptosis, angiogenic actions, regulation of ion channels, and even crosstalk with nitric oxide. In virtue of the heightened enthusiasm, novel H2S-releasing agents have been developed and others have been characterized from plant sources. Though enormous efforts have been made, many aspects remain unclear and further research is necessary.

Therefore, this Special Issue calls for original research as well as reviews, including perspectives from the field on the current standing of the research into the role of endogenous H2S in the development of cardiovascular diseases or disorders promoting cardiovascular diseases, such as endothelial dysfunction or atherosclerosis. Moreover, the therapeutic potential of naturally or synthetically derived H2S donors in cardiovascular diseases is of interest. Reviews and original research providing insight into molecular mechanisms underlying the action of H2S and H2S-releasing agents in cardiovascular system, which may promote the knowledge and lead to new therapeutic targets, are also welcome.

Prof. Lara Testai
Prof. Vincenzo Calderone
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

  • Hydrogen sulfide
  • H2S-releasing agents
  • Cardiovascular diseases
  • H2S signaling pathway
  • Metabolic disorders
  • Ageing
  • Antioxidant effects
  • Anti-inflammatory effects
  • Potassium channels
  • Mitochondrial biogenesis

Published Papers (8 papers)

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Research

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16 pages, 2253 KiB  
Article
The H2S-Donor Erucin Exhibits Protective Effects against Vascular Inflammation in Human Endothelial and Smooth Muscle Cells
by Alma Martelli, Eugenia Piragine, Era Gorica, Valentina Citi, Lara Testai, Eleonora Pagnotta, Luca Lazzeri, Nicola Pecchioni, Valerio Ciccone, Rosangela Montanaro, Lorenzo Di Cesare Mannelli, Carla Ghelardini, Vincenzo Brancaleone, Lucia Morbidelli and Vincenzo Calderone
Antioxidants 2021, 10(6), 961; https://doi.org/10.3390/antiox10060961 - 15 Jun 2021
Cited by 24 | Viewed by 3537
Abstract
Preservation of vascular wall integrity against degenerative processes associated with ageing, fat-rich diet and metabolic diseases is a timely therapeutical challenge. The loss of endothelial function and integrity leads to cardiovascular diseases and multiorgan inflammation. The protective effects of the H2S-donor [...] Read more.
Preservation of vascular wall integrity against degenerative processes associated with ageing, fat-rich diet and metabolic diseases is a timely therapeutical challenge. The loss of endothelial function and integrity leads to cardiovascular diseases and multiorgan inflammation. The protective effects of the H2S-donor erucin, an isothiocyanate purified by Eruca sativa Mill. seeds, were evaluated on human endothelial and vascular smooth muscle cells. In particular, erucin actions were evaluated on cell viability, ROS, caspase 3/7, inflammatory markers levels and the endothelial hyperpermeability in an inflammatory model associated with high glucose concentrations (25 mM, HG). Erucin significantly prevented the HG-induced decrease in cell viability as well as the increase in ROS, caspase 3/7 activation, and TNF-α and IL-6 levels. Similarly, erucin suppressed COX-2 and NF-κB upregulation associated with HG exposure. Erucin also caused a significant inhibition of p22phox subunit expression in endothelial cells. In addition, erucin significantly prevented the HG-induced increase in endothelial permeability as also confirmed by the quantification of the specific markers VE-Cadherin and ZO-1. In conclusion, our results assess anti-inflammatory and antioxidant effects by erucin in vascular cells undergoing HG-induced inflammation and this protection parallels the preservation of endothelial barrier properties. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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15 pages, 2101 KiB  
Article
Uterine Dysfunction in Diabetic Mice: The Role of Hydrogen Sulfide
by Emma Mitidieri, Domenico Vanacore, Carlotta Turnaturi, Raffaella Sorrentino and Roberta d’Emmanuele di Villa Bianca
Antioxidants 2020, 9(10), 917; https://doi.org/10.3390/antiox9100917 - 26 Sep 2020
Cited by 6 | Viewed by 1971
Abstract
It is well-known that the physiological uterine peristalsis, related to several phases of reproductive functions, plays a pivotal role in fertility and female reproductive health. Here, we have addressed the role of hydrogen sulfide (H2S) signaling in changes of uterine contractions [...] Read more.
It is well-known that the physiological uterine peristalsis, related to several phases of reproductive functions, plays a pivotal role in fertility and female reproductive health. Here, we have addressed the role of hydrogen sulfide (H2S) signaling in changes of uterine contractions driven by diabetes in non-obese diabetic (NOD) mice, a murine model of type-1 diabetes mellitus. The isolated uterus of NOD mice showed a significant reduction in spontaneous motility coupled to a generalized hypo-contractility to uterotonic agents. The levels of cyclic nucleotides, cAMP and cGMP, notoriously involved in the regulation of uterus homeostasis, were significantly elevated in NOD mouse uteri. This increase was well-correlated with the higher levels of H2S, a non-specific endogenous inhibitor of phosphodiesterases. The exposure of isolated uterus to L-cysteine (L-Cys), but not to sodium hydrogen sulfide, the exogenous source of H2S, showed a weak tocolytic effect in the uterus of NOD mice. Western blot analysis revealed a reorganization of the enzymatic expression with an upregulation of 3-mercaptopyruvate-sulfurtransferase (3-MST) coupled to a reduction in both cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) expression. In conclusion, the increased levels of cyclic nucleotides dysregulate the uterus peristalsis and contractility in diabetic mice through an increase in basal H2S synthesis suggesting a role of 3-MST. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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Review

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23 pages, 1986 KiB  
Review
Modulation of EndMT by Hydrogen Sulfide in the Prevention of Cardiovascular Fibrosis
by Lara Testai, Vincenzo Brancaleone, Lorenzo Flori, Rosangela Montanaro and Vincenzo Calderone
Antioxidants 2021, 10(6), 910; https://doi.org/10.3390/antiox10060910 - 03 Jun 2021
Cited by 28 | Viewed by 4538
Abstract
Endothelial mesenchymal transition (EndMT) has been described as a fundamental process during embryogenesis; however, it can occur also in adult age, underlying pathological events, including fibrosis. Indeed, during EndMT, the endothelial cells lose their specific markers, such as vascular endothelial cadherin (VE-cadherin), and [...] Read more.
Endothelial mesenchymal transition (EndMT) has been described as a fundamental process during embryogenesis; however, it can occur also in adult age, underlying pathological events, including fibrosis. Indeed, during EndMT, the endothelial cells lose their specific markers, such as vascular endothelial cadherin (VE-cadherin), and acquire a mesenchymal phenotype, expressing specific products, such as α-smooth muscle actin (α-SMA) and type I collagen; moreover, the integrity of the endothelium is disrupted, and cells show a migratory, invasive and proliferative phenotype. Several stimuli can trigger this transition, but transforming growth factor (TGF-β1) is considered the most relevant. EndMT can proceed in a canonical smad-dependent or non-canonical smad-independent manner and ultimately regulate gene expression of pro-fibrotic machinery. These events lead to endothelial dysfunction and atherosclerosis at the vascular level as well as myocardial hypertrophy and fibrosis. Indeed, EndMT is the mechanism which promotes the progression of cardiovascular disorders following hypertension, diabetes, heart failure and also ageing. In this scenario, hydrogen sulfide (H2S) has been widely described for its preventive properties, but its role in EndMT is poorly investigated. This review is focused on the evaluation of the putative role of H2S in the EndMT process. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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21 pages, 1233 KiB  
Review
Endothelium as a Source and Target of H2S to Improve Its Trophism and Function
by Valerio Ciccone, Shirley Genah and Lucia Morbidelli
Antioxidants 2021, 10(3), 486; https://doi.org/10.3390/antiox10030486 - 19 Mar 2021
Cited by 25 | Viewed by 3797
Abstract
The vascular endothelium consists of a single layer of squamous endothelial cells (ECs) lining the inner surface of blood vessels. Nowadays, it is no longer considered as a simple barrier between the blood and vessel wall, but a central hub to control blood [...] Read more.
The vascular endothelium consists of a single layer of squamous endothelial cells (ECs) lining the inner surface of blood vessels. Nowadays, it is no longer considered as a simple barrier between the blood and vessel wall, but a central hub to control blood flow homeostasis and fulfill tissue metabolic demands by furnishing oxygen and nutrients. The endothelium regulates the proper functioning of vessels and microcirculation, in terms of tone control, blood fluidity, and fine tuning of inflammatory and redox reactions within the vessel wall and in surrounding tissues. This multiplicity of effects is due to the ability of ECs to produce, process, and release key modulators. Among these, gasotransmitters such as nitric oxide (NO) and hydrogen sulfide (H2S) are very active molecules constitutively produced by endotheliocytes for the maintenance and control of vascular physiological functions, while their impairment is responsible for endothelial dysfunction and cardiovascular disorders such as hypertension, atherosclerosis, and impaired wound healing and vascularization due to diabetes, infections, and ischemia. Upregulation of H2S producing enzymes and administration of H2S donors can be considered as innovative therapeutic approaches to improve EC biology and function, to revert endothelial dysfunction or to prevent cardiovascular disease progression. This review will focus on the beneficial autocrine/paracrine properties of H2S on ECs and the state of the art on H2S potentiating drugs and tools. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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13 pages, 848 KiB  
Review
Hydrogen Sulfide as a Potential Therapy for Heart Failure—Past, Present, and Future
by Kyle B. LaPenna, David J. Polhemus, Jake E. Doiron, Hunter A. Hidalgo, Zhen Li and David J. Lefer
Antioxidants 2021, 10(3), 485; https://doi.org/10.3390/antiox10030485 - 19 Mar 2021
Cited by 20 | Viewed by 3153
Abstract
Hydrogen sulfide (H2S) is an endogenous, gaseous signaling molecule that plays a critical role in cardiac and vascular biology. H2S regulates vascular tone and oxidant defenses and exerts cytoprotective effects in the heart and circulation. Recent studies indicate that [...] Read more.
Hydrogen sulfide (H2S) is an endogenous, gaseous signaling molecule that plays a critical role in cardiac and vascular biology. H2S regulates vascular tone and oxidant defenses and exerts cytoprotective effects in the heart and circulation. Recent studies indicate that H2S modulates various components of metabolic syndrome, including obesity and glucose metabolism. This review will discuss studies exhibiting H2S -derived cardioprotective signaling in heart failure with reduced ejection fraction (HFrEF). We will also discuss the role of H2S in metabolic syndrome and heart failure with preserved ejection fraction (HFpEF). Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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27 pages, 8039 KiB  
Review
Trends in H2S-Donors Chemistry and Their Effects in Cardiovascular Diseases
by Angela Corvino, Francesco Frecentese, Elisa Magli, Elisa Perissutti, Vincenzo Santagada, Antonia Scognamiglio, Giuseppe Caliendo, Ferdinando Fiorino and Beatrice Severino
Antioxidants 2021, 10(3), 429; https://doi.org/10.3390/antiox10030429 - 11 Mar 2021
Cited by 39 | Viewed by 3939
Abstract
Hydrogen sulfide (H2S) is an endogenous gasotransmitter recently emerged as an important regulatory mediator of numerous human cell functions in health and in disease. In fact, much evidence has suggested that hydrogen sulfide plays a significant role in many physio-pathological processes, [...] Read more.
Hydrogen sulfide (H2S) is an endogenous gasotransmitter recently emerged as an important regulatory mediator of numerous human cell functions in health and in disease. In fact, much evidence has suggested that hydrogen sulfide plays a significant role in many physio-pathological processes, such as inflammation, oxidation, neurophysiology, ion channels regulation, cardiovascular protection, endocrine regulation, and tumor progression. Considering the plethora of physiological effects of this gasotransmitter, the protective role of H2S donors in different disease models has been extensively studied. Based on the growing interest in H2S-releasing compounds and their importance as tools for biological and pharmacological studies, this review is an exploration of currently available H2S donors, classifying them by the H2S-releasing-triggered mechanism and highlighting those potentially useful as promising drugs in the treatment of cardiovascular diseases. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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20 pages, 1497 KiB  
Review
Harnessing the Benefits of Endogenous Hydrogen Sulfide to Reduce Cardiovascular Disease
by Kevin M. Casin and John W. Calvert
Antioxidants 2021, 10(3), 383; https://doi.org/10.3390/antiox10030383 - 04 Mar 2021
Cited by 12 | Viewed by 3484
Abstract
Cardiovascular disease is the leading cause of death in the U.S. While various studies have shown the beneficial impact of exogenous hydrogen sulfide (H2S)-releasing drugs, few have demonstrated the influence of endogenous H2S production. Modulating the predominant enzymatic sources [...] Read more.
Cardiovascular disease is the leading cause of death in the U.S. While various studies have shown the beneficial impact of exogenous hydrogen sulfide (H2S)-releasing drugs, few have demonstrated the influence of endogenous H2S production. Modulating the predominant enzymatic sources of H2S—cystathionine-β-synthase, cystathionine-γ-lyase, and 3-mercaptopyruvate sulfurtransferase—is an emerging and promising research area. This review frames the discussion of harnessing endogenous H2S within the context of a non-ischemic form of cardiomyopathy, termed diabetic cardiomyopathy, and heart failure. Also, we examine the current literature around therapeutic interventions, such as intermittent fasting and exercise, that stimulate H2S production. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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19 pages, 2966 KiB  
Review
Preventing Developmental Origins of Cardiovascular Disease: Hydrogen Sulfide as a Potential Target?
by Chien-Ning Hsu and You-Lin Tain
Antioxidants 2021, 10(2), 247; https://doi.org/10.3390/antiox10020247 - 05 Feb 2021
Cited by 23 | Viewed by 3128
Abstract
The cardiovascular system can be programmed by a diversity of early-life insults, leading to cardiovascular disease (CVD) in adulthood. This notion is now termed developmental origins of health and disease (DOHaD). Emerging evidence indicates hydrogen sulfide (H2S), a crucial regulator of [...] Read more.
The cardiovascular system can be programmed by a diversity of early-life insults, leading to cardiovascular disease (CVD) in adulthood. This notion is now termed developmental origins of health and disease (DOHaD). Emerging evidence indicates hydrogen sulfide (H2S), a crucial regulator of cardiovascular homeostasis, plays a pathogenetic role in CVD of developmental origins. Conversely, early H2S-based interventions have proved beneficial in preventing adult-onset CVD in animal studies via reversing programming processes by so-called reprogramming. The focus of this review will first summarize the current knowledge on H2S implicated in cardiovascular programming. This will be followed by supporting evidence for the links between H2S signaling and underlying mechanisms of cardiovascular programming, such as oxidative stress, nitric oxide deficiency, dysregulated nutrient-sensing signals, activation of the renin–angiotensin system, and gut microbiota dysbiosis. It will also provide an overview from animal models regarding how H2S-based reprogramming interventions, such as precursors of H2S and H2S donors, may prevent CVD of developmental origins. A better understanding of cardiovascular programming and recent advances in H2S-based interventions might provide the answers to bring down the global burden of CVD. Full article
(This article belongs to the Special Issue Protective Effects of H2S and H2S-Releasing Drugs in Cardiovascular Diseases)
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