scholarly journals Harnessing the Benefits of Endogenous Hydrogen Sulfide to Reduce Cardiovascular Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 383
Author(s):  
Kevin M. Casin ◽  
John W. Calvert
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Research Area ◽  
Therapeutic Interventions ◽  
Intermittent Fasting ◽  
Beneficial Impact ◽  
Mercaptopyruvate Sulfurtransferase ◽  
H2s Production ◽  
The U.S

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.

scholarly journals The Drug Developments of Hydrogen Sulfide on Cardiovascular Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-21 ◽  
Author(s):  
Ya-Dan Wen ◽  
Hong Wang ◽  
Yi-Zhun Zhu
Keyword(s):  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Molecular Mechanisms ◽  
Pathological Process ◽  
The Other ◽  
Acid Oxidase ◽  
Organosulfur Compounds ◽  
Amino Acid Oxidase ◽  
Mercaptopyruvate Sulfurtransferase ◽  
The One

The recognition of hydrogen sulfide (H2S) has been evolved from a toxic gas to a physiological mediator, exhibiting properties similar to NO and CO. On the one hand, H2S is produced from L-cysteine by enzymes of cystathionineγ-lyase (CSE) and cystathionineβ-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST) in combination with aspartate aminotransferase (AAT) (also called as cysteine aminotransferase, CAT); on the other hand, H2S is produced from D-cysteine by enzymes of D-amino acid oxidase (DAO). Besides sulfide salt, several sulfide-releasing compounds have been synthesized, including organosulfur compounds, Lawesson’s reagent and analogs, and plant-derived natural products. Based on garlic extractions, we synthesized S-propargyl-L-cysteine (SPRC) and its analogs to contribute our endeavors on drug development of sulfide-containing compounds. A multitude of evidences has presented H2S is widely involved in the roles of physiological and pathological process, including hypertension, atherosclerosis, angiogenesis, and myocardial infarcts. This review summarizes current sulfide compounds, available H2S measurements, and potential molecular mechanisms involved in cardioprotections to help researchers develop further applications and therapeutically drugs.

scholarly journals Phenotypic Shifts in Neurons of the Dorsal Motor Nucleus of the Vagus Resulting from Chronic Cardiac Ischemia

2020 ◽  
Author(s):  
Jonathan Gorky ◽  
Rajanikanth Vadigepalli ◽  
James Schwaber
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Single Cells ◽  
Therapeutic Interventions ◽  
Motor Nucleus ◽  
Vagal Activity ◽  
Autonomic Nervous ◽  
Dorsal Motor Nucleus

AbstractHeart disease remains the number one cause of mortality in the world in spite of significant efforts aimed at treatment. The use of vagal stimulation in the treatment of heart failure has shown mixed successes (Dicarlo et al. 2013; Zannad et al. 2015), suggesting that the treatment has potential, but that the mechanism incompletely understood. Vagal activity confers a robust cardioprotective effect in both humans and animal models, preferentially originating specifically from the dorsal motor nucleus of the vagus (DMV) and deriving a significant benefit from intact gut projections, not just cardiac (Shinlapawittayatorn et al. 2013; Mastitskaya et al. 2012; Basalay et al. 2012). In order to examine the DMV response to heart failure, myocardial infarction was induced in male Sprague Dawley rats. DMV neurons were isolated in small pools of single cells using laser capture microdissection 1 week and 3 weeks after infarction and their gene expression assayed. The results show a transcriptional shift towards a neurosecretory phenotype starting at 1 week and increasing in recruitment of neurons to 3 weeks. The LAD ligation shift appears mediated in part by upregulation of Pax4a, a transcription factor most active during stem cell development of neurosecretory cells during embryonic development. This phenotype is characterized by upregulation of Cacna1d (Cav1.3) and Hcn2 along with increased expression of Cck and Sst. This work suggests that the neurons of the DMV adaptively respond to the dynamics present in the periphery, elucidating the means by which the nature of vagal activity responds to heart failure.Significance StatementThe autonomic nervous system plays a significant role in the pathogenesis of cardiovascular disease. Through demonstration of shifting neuronal phenotypes in central neurons in response to peripheral stimuli, we suggest that neuron peptide or neurotransmitter phenotypes are not static in adult rodents. This suggests that even “reflexes” are modifiable dynamic systems. With such plasticity in the transcriptional programming existing in autonomic brain regions there can be new potential therapeutic interventions for cardiovascular disease aimed at leveraging the autonomic nervous system.

scholarly journals Myocardial Protective Effect of Gas Signal Molecule Hydrogen Sulfide on Cardiovascular Disease

2020 ◽  
Vol 3 (3) ◽  
pp. 12
Author(s):  
Lijuan Li ◽  
Fei Zou
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Cardiovascular Diseases ◽  
Protective Effect ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Signal Molecule ◽  
Neuroactive Substance ◽  
New Type

Cardiovascular diseases increase continually in the worldwide scale, and its specific pathogenesis has not been completely clear. The gas signal molecule hydrogen sulfide (H2S) is a new type of neuroactive substance, which plays many biological roles in many systems such as cardiovascular system. In recent years, a lot of research has confirmed H2S has myocardial protective effect on cardiovascular diseases such as atherosclerosis, ischemia-reperfusion injury, hypertension and heart failure. This paper reviews the research status of myocardial protective effect of H2S on cardiovascular diseases.

scholarly journals Hydrogen Sulfide (H2S) and Polysulfide (H2Sn) Signaling: The First 25 Years

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 896
Author(s):  
Hideo Kimura
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Research Area ◽  
Cytoprotective Effect ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Energy Formation ◽  
New Research ◽  
The Brain ◽  
Activity Energy

Since the first description of hydrogen sulfide (H2S) as a toxic gas in 1713 by Bernardino Ramazzini, most studies on H2S have concentrated on its toxicity. In 1989, Warenycia et al. demonstrated the existence of endogenous H2S in the brain, suggesting that H2S may have physiological roles. In 1996, we demonstrated that hydrogen sulfide (H2S) is a potential signaling molecule, which can be produced by cystathionine β-synthase (CBS) to modify neurotransmission in the brain. Subsequently, we showed that H2S relaxes vascular smooth muscle in synergy with nitric oxide (NO) and that cystathionine γ-lyase (CSE) is another producing enzyme. This study also opened up a new research area of a crosstalk between H2S and NO. The cytoprotective effect, anti-inflammatory activity, energy formation, and oxygen sensing by H2S have been subsequently demonstrated. Two additional pathways for the production of H2S with 3-mercaptopyruvate sulfurtransferase (3MST) from l- and d-cysteine have been identified. We also discovered that hydrogen polysulfides (H2Sn, n ≥ 2) are potential signaling molecules produced by 3MST. H2Sn regulate the activity of ion channels and enzymes, as well as even the growth of tumors. S-Sulfuration (S-sulfhydration) proposed by Snyder is the main mechanism for H2S/H2Sn underlying regulation of the activity of target proteins. This mini review focuses on the key findings on H2S/H2Sn signaling during the first 25 years.

scholarly journals Kidney Ischemia-Reperfusion Decreases Hydrogen Sulfide and Increases Oxidative Stress in the Heart

Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1565
Author(s):  
Charith U. B. Wijerathne ◽  
Susara Madduma Hewage ◽  
Yaw L. Siow ◽  
Karmin O
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Underlying Mechanism ◽  
Sprague Dawley ◽  
Increased Risk ◽  
H2s Production ◽  
Kidney Ischemia

Patients with acute kidney injury (AKI) have an increased risk of cardiovascular disease. The underlying mechanism of AKI-induced heart injury is not well-understood. Hydrogen sulfide (H2S), at physiological concentrations, has been implicated in cardiovascular protection through redox balance and vessel relaxation. Cystathionine gamma-lyase (CSE) plays an essential role in H2S production in the heart. The present study investigated the effect of AKI on H2S production and oxidative stress in the heart. AKI was induced by kidney ischemia-reperfusion in male and female Sprague-Dawley rats, which led to an increase in plasma creatinine and blood urea nitrogen levels. There was a significant increase in lipid peroxidation and a decrease in glutathione (antioxidant) levels in the plasma and heart, indicating systemic and cardiac oxidative stress. Kidney ischemia-reperfusion reduced CSE expression and H2S production in the heart. There was a decrease in antioxidant transcription factor Nrf2 level in the nucleus and an increase in inflammatory cytokine (IL-6, TNF-α) expression in the heart. These results suggest that AKI can down-regulate CSE-mediated H2S production, reduce glutathione levels and increase oxidative stress in the heart. This may contribute to an increased risk of cardiovascular disease in AKI.

scholarly journals The capacity to produce hydrogen sulfide (H2S) via cysteine degradation is ubiquitous in the human gut microbiome

2021 ◽  
Author(s):  
Domenick J Braccia ◽  
Xiaofang Jiang ◽  
Mihai Pop ◽  
Brantley Hall
Keyword(s):  
Hydrogen Sulfide ◽  
Gut Microbiome ◽  
Bacterial Species ◽  
Therapeutic Interventions ◽  
Metagenomic Data ◽  
Human Gut ◽  
Gut Microbes ◽  
Human Gut Microbiome ◽  
Degrading Bacteria ◽  
H2s Production

As one of the three mammalian gasotransmitters, hydrogen sulfide (H2S) plays a major role in maintaining physiological homeostasis. Endogenously produced H2S plays numerous beneficial roles including mediating vasodilation and conferring neuroprotection. Due to its high membrane permeability, exogenously produced H2S originating from the gut microbiota can also influence human physiology and is implicated in reducing intestinal mucosal integrity and potentiating genotoxicity and is therefore a potential target for therapeutic interventions. Gut microbial H2S production is often attributed to dissimilatory sulfate reducers such as Desulfovibrio and Bilophila species. However, an alternative source for H2S production, cysteine degradation, is present in gut microbes, but the genes responsible for cysteine degradation have not been systematically annotated in gut microbes. To better understand the potential for H2S production via cysteine degradation by the human gut microbiome, we performed a comprehensive search for genes encoding cysteine-degrading genes in 4,644 bacterial genomes from the Unified Human Gastrointestinal Genome (UHGG) catalogue. We identified 407 gut bacterial species as putative cysteine degrading bacteria, 328 of which have not been previously implicated in H2S production. We identified the presence of at least one putative cysteine degrading bacteria in metagenomic data of 100% of 6,644 healthy subjects and the expression of cysteine-degrading genes in metatranscriptomics data of 100% of 59 samples. Additionally, putative cysteine-degrading bacteria are more abundant than sulfate reducing bacteria (p<2.2e-16). Overall, this study improves our understanding of the capacity for H2S production by the human gut microbiome and may help to inform interventions to therapeutically modulate gut microbial H2S production.

Exercise, cardiovascular disease, and chronic heart failure

2001 ◽  
Vol 82 (3B) ◽  
pp. 0s76-0s81 ◽  
Author(s):  
Reed Humphrey ◽  
Matthew N. Bartels
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Chronic Heart Failure

The Safety of Linagliptin vs. Other Antidiabetic Agents with Regard to the Risk of Heart Failure Hospitalization in Routine Care in the U.S.

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2364-PUB
Author(s):  
ELISABETTA PATORNO ◽  
MUFADDAL MAHESRI ◽  
CHANDRASEKAR GOPALAKRISHNAN ◽  
KIMBERLY BRODOVICZ ◽  
ANDREA MEYERS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Routine Care ◽  
Heart Failure Hospitalization ◽  
Antidiabetic Agents ◽  
The U.S

NT-PROBNP AND THE CUT-OFF VALUE IN CARDIOVASCULAR DISEASES

2011 ◽  
pp. 5-12
Author(s):  
Anh Tien Hoang ◽  
Van Minh Huynh ◽  
Khanh Hoang ◽  
Huu Dang Tran ◽  
Viet An Tran
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Pilot Study ◽  
Cardiovascular Diseases ◽  
Clinical Application ◽  
European Society ◽  
The Other ◽  
Cardiac Marker ◽  
Cardiac Biomarker ◽  
European Society Of Cardiology

NT-ProBNP is a high value cardiac biomarker and widely applies in many cardiovascular diseases. The evaluation of concentration of NT-ProBNP needs the concern about age, gender, obesity and especially we need each cut-off point for each cause of cardiovascular disease in evaluation and clinical application. Because NT-ProBNP is a new cardiac marker and has been researched in 5 recent years, the cut-off of NT-ProBNP is still being studied for the clinical application in cardiovascular diseases. Only the cut-off of NT-ProBNP in diagnosis heart failure was guided by European Society of Cardiology. The meaning of introduce cut-off value of value plays an role as pilot study for the other relate study and brings the NT-ProBNP closely approach to clinical application.

scholarly journals Late-life intermittent fasting decreases aging-related frailty and increases renal hydrogen sulfide production in a sexually dimorphic manner

GeroScience ◽  
2021 ◽  
Author(s):  
Yoko O. Henderson ◽  
Nazmin Bithi ◽  
Christopher Link ◽  
Jie Yang ◽  
Rebecca Schugar ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Dietary Intervention ◽  
Caloric Intake ◽  
Production Capacity ◽  
Late Life ◽  
Model Organisms ◽  
Intermittent Fasting ◽  
Sexually Dimorphic ◽  
Average Life Expectancy ◽  
Multiple Components

AbstractGlobal average life expectancy continues to rise. As aging increases the likelihood of frailty, which encompasses metabolic, musculoskeletal, and cognitive deficits, there is a need for effective anti-aging treatments. It is well established in model organisms that dietary restriction (DR), such as caloric restriction or protein restriction, enhances health and lifespan. However, DR is not widely implemented in the clinic due to patient compliance and its lack of mechanistic underpinnings. Thus, the present study tested the effects of a somewhat more clinically applicable and adoptable DR regimen, every-other-day (EOD) intermittent fasting, on frailty in 20-month-old male and female C57BL/6 mice. Frailty was determined by a series of metabolic, musculoskeletal, and cognitive tasks performed prior to and toward the end of the 2.5-month dietary intervention. Late-life EOD fasting attenuated overall energy intake, hypothalamic inflammatory gene expression, and frailty in males. However, it failed to reduce overall caloric intake and had a little positive effect in females. Given that the selected benefits of DR are dependent on augmented production of the gasotransmitter hydrogen sulfide (H2S) and that renal H2S production declines with age, we tested the effects of EOD fasting on renal H2S production capacity and its connection to frailty in males. EOD fasting boosted renal H2S production, which positively correlated with improvements in multiple components of frailty tasks. Therefore, late-life initiated EOD fasting is sufficient to reduce aging-related frailty, at least in males, and suggests that renal H2S production capacity may modulate the effects of late-life EOD fasting on frailty.

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