scholarly journals The Role of Hydrogen Sulfide in Respiratory Diseases

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 682
Author(s):  
Saadullah Khattak ◽  
Qian-Qian Zhang ◽  
Muhammad Sarfraz ◽  
Pir Muhammad ◽  
Ebenezeri Erasto Ngowi ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Respiratory Diseases ◽  
Therapeutic Potential ◽  
Pulmonary Inflammation ◽  
Cellular Functions ◽  
Comprehensive Overview ◽  
Therapeutic Role ◽  
Diverse Range ◽  
Incidence And Mortality

Respiratory diseases are leading causes of death and disability around the globe, with a diverse range of health problems. Treatment of respiratory diseases and infections has been verified to be thought-provoking because of the increasing incidence and mortality rate. Hydrogen sulfide (H2S) is one of the recognized gaseous transmitters involved in an extensive range of cellular functions, and physiological and pathological processes in a variety of diseases, including respiratory diseases. Recently, the therapeutic potential of H2S for respiratory diseases has been widely investigated. H2S plays a vital therapeutic role in obstructive respiratory disease, pulmonary fibrosis, emphysema, pancreatic inflammatory/respiratory lung injury, pulmonary inflammation, bronchial asthma and bronchiectasis. Although the therapeutic role of H2S has been extensively studied in various respiratory diseases, a concrete literature review will have an extraordinary impact on future therapeutics. This review provides a comprehensive overview of the effective role of H2S in respiratory diseases. Besides, we also summarized H2S production in the lung and its metabolism processes in respiratory diseases.

Hydrogen sulfide-mediated cardioprotection: mechanisms and therapeutic potential

2010 ◽  
Vol 120 (6) ◽  
pp. 219-229 ◽  
Author(s):  
Madhav Lavu ◽  
Shashi Bhushan ◽  
David J. Lefer
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Therapeutic Potential ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Signalling Molecule ◽  
Anti Inflammatory ◽  
Antioxidant Effects

H2S (hydrogen sulfide), viewed with dread for more than 300 years, is rapidly becoming a ubiquitously present and physiologically relevant signalling molecule. Knowledge of the production and metabolism of H2S has spurred interest in delineating its functions both in physiology and pathophysiology of disease. Although its role in blood pressure regulation and interaction with NO is controversial, H2S, through its anti-apoptotic, anti-inflammatory and antioxidant effects, has demonstrated significant cardioprotection. As a result, a number of sulfide-donor drugs, including garlic-derived polysulfides, are currently being designed and investigated for the treatment of cardiovascular conditions, specifically myocardial ischaemic disease. However, huge gaps remain in our knowledge about this gasotransmitter. Only by additional studies will we understand more about the role of this intriguing molecule in the treatment of cardiovascular disease.

scholarly journals Recent progress in research on molecular mechanisms of autophagy in the heart

2015 ◽  
Vol 308 (4) ◽  
pp. H259-H268 ◽  
Author(s):  
Yasuhiro Maejima ◽  
Yun Chen ◽  
Mitsuaki Isobe ◽  
Åsa B. Gustafsson ◽  
Richard N. Kitsis ◽  
...  
Keyword(s):  
Heart Disease ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Degradation Process ◽  
Structure And Function ◽  
Cellular Functions ◽  
Evolutionarily Conserved ◽  
And Function ◽  
Cellular Dysfunction

Dysregulation of autophagy, an evolutionarily conserved process for degradation of long-lived proteins and organelles, has been implicated in the pathogenesis of human disease. Recent research has uncovered pathways that control autophagy in the heart and molecular mechanisms by which alterations in this process affect cardiac structure and function. Although initially thought to be a nonselective degradation process, autophagy, as it has become increasingly clear, can exhibit specificity in the degradation of molecules and organelles, such as mitochondria. Furthermore, it has been shown that autophagy is involved in a wide variety of previously unrecognized cellular functions, such as cell death and metabolism. A growing body of evidence suggests that deviation from appropriate levels of autophagy causes cellular dysfunction and death, which in turn leads to heart disease. Here, we review recent advances in understanding the role of autophagy in heart disease, highlight unsolved issues, and discuss the therapeutic potential of modulating autophagy in heart disease.

Vitamin D/VDR in acute kidney injury: a potential therapeutic target

2020 ◽  
Vol 27 ◽  
Author(s):  
Siqing Jiang ◽  
Lihua Huang ◽  
Wei Zhang ◽  
Hao Zhang
Keyword(s):  
Vitamin D ◽  
Acute Kidney Injury ◽  
Therapeutic Target ◽  
Poor Prognosis ◽  
Therapeutic Potential ◽  
Kidney Injury ◽  
Potential Therapeutic Target ◽  
Promising Therapeutic Target ◽  
Incidence And Mortality

: Despite many strategies and parameters used in clinical practice, the incidence and mortality of acute kidney injury (AKI) are still high with poor prognosis. With the development of molecular biology, the role of vitamin D and vitamin D receptor (VDR) in AKI is drawing increasing attention. Accumulated researches have suggested that Vitamin D deficiency is a risk factor of both clinical and experimental AKI, and vitamin D/VDR could be a promising therapeutic target against AKI. However, more qualitative clinical researches are needed to provide stronger evidence for clinical application of vitamin D and VDR agonists in the future. Issues like the route and dosage of administration also await more attention. The present review aims to summarize the current works on the role of vitamin D/VDR in AKI and try to provide some new insight of its therapeutic potential.

scholarly journals Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1051 ◽  
Author(s):  
Xiaomeng Shi ◽  
Hongyu Qiu
Keyword(s):  
Therapeutic Potential ◽  
Heart Diseases ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Cardiac Protection ◽  
Cellular Functions ◽  
Post Translational Modifications ◽  
Cellular Redox ◽  
Novel Therapeutic Strategies

Like other post-translational modifications (PTMs) of proteins, S-nitrosylation has been considered a key regulatory mechanism of multiple cellular functions in many physiological and disease conditions. Emerging evidence has demonstrated that S-nitrosylation plays a crucial role in regulating redox homeostasis in the stressed heart, leading to discoveries in the mechanisms underlying the pathogenesis of heart diseases and cardiac protection. In this review, we summarize recent studies in understanding the molecular and biological basis of S-nitrosylation, including the formation, spatiotemporal specificity, homeostatic regulation, and association with cellular redox status. We also outline the currently available methods that have been applied to detect S-nitrosylation. Additionally, we synopsize the up-to-date studies of S-nitrosylation in various cardiac diseases in humans and animal models, and we discuss its therapeutic potential in cardiac protection. These pieces of information would bring new insights into understanding the role of S-nitrosylation in cardiac pathogenesis and provide novel avenues for developing novel therapeutic strategies for heart diseases.

scholarly journals CDK9: A Comprehensive Review of Its Biology, and Its Role as a Potential Target for Anti-Cancer Agents

2021 ◽  
Vol 11 ◽  
Author(s):  
Abel Tesfaye Anshabo ◽  
Robert Milne ◽  
Shudong Wang ◽  
Hugo Albrecht
Keyword(s):  
Therapeutic Potential ◽  
Continuous Production ◽  
Clinical Settings ◽  
Cellular Functions ◽  
Cyclin Dependent Kinases ◽  
Solid Malignancies ◽  
Wide Range ◽  
Hematological Cancers ◽  
Anti Cancer

Cyclin-dependent kinases (CDKs) are proteins pivotal to a wide range of cellular functions, most importantly cell division and transcription, and their dysregulations have been implicated as prominent drivers of tumorigenesis. Besides the well-established role of cell cycle CDKs in cancer, the involvement of transcriptional CDKs has been confirmed more recently. Most cancers overtly employ CDKs that serve as key regulators of transcription (e.g., CDK9) for a continuous production of short-lived gene products that maintain their survival. As such, dysregulation of the CDK9 pathway has been observed in various hematological and solid malignancies, making it a valuable anticancer target. This therapeutic potential has been utilized for the discovery of CDK9 inhibitors, some of which have entered human clinical trials. This review provides a comprehensive discussion on the structure and biology of CDK9, its role in solid and hematological cancers, and an updated review of the available inhibitors currently being investigated in preclinical and clinical settings.

scholarly journals The Role of Innate Lymphoid Cells in Chronic Respiratory Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Amy T. Hsu ◽  
Timothy A. Gottschalk ◽  
Evelyn Tsantikos ◽  
Margaret L. Hibbs
Keyword(s):  
Immune System ◽  
Respiratory Diseases ◽  
Pulmonary Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Chronic Respiratory Diseases ◽  
Chronic Lung Diseases ◽  
Pulmonary Immune System

The lung is a vital mucosal organ that is constantly exposed to the external environment, and as such, its defenses are continuously under threat. The pulmonary immune system has evolved to sense and respond to these danger signals while remaining silent to innocuous aeroantigens. The origin of the defense system is the respiratory epithelium, which responds rapidly to insults by the production of an array of mediators that initiate protection by directly killing microbes, activating tissue-resident immune cells and recruiting leukocytes from the blood. At the steady-state, the lung comprises a large collection of leukocytes, amongst which are specialized cells of lymphoid origin known as innate lymphoid cells (ILCs). ILCs are divided into three major helper-like subsets, ILC1, ILC2 and ILC3, which are considered the innate counterparts of type 1, 2 and 17 T helper cells, respectively, in addition to natural killer cells and lymphoid tissue inducer cells. Although ILCs represent a small fraction of the pulmonary immune system, they play an important role in early responses to pathogens and facilitate the acquisition of adaptive immunity. However, it is now also emerging that these cells are active participants in the development of chronic lung diseases. In this mini-review, we provide an update on our current understanding of the role of ILCs and their regulation in the lung. We summarise how these cells and their mediators initiate, sustain and potentially control pulmonary inflammation, and their contribution to the respiratory diseases chronic obstructive pulmonary disease (COPD) and asthma.

CLINICAL AND THERAPEUTIC VALUE OF ADIPOKINES IN PATIENTS WITH CHRONIC KIDNEY DISEASE

2020 ◽  
pp. 5-9
Author(s):  
Ya. M Fylenko
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Adipose Tissue ◽  
Kidney Disease ◽  
Therapeutic Potential ◽  
Interdisciplinary Approach ◽  
Blood Lipid ◽  
The Body ◽  
Incidence And Mortality

This review is devoted to the analysis of the role of adipokines in formation of pathological changes in renal function and structure. The patients with chronic kidney disease have a high risk of cardiovascular disease. Currently, the role of systemic hormonal and metabolic factors in the pathogenesis of the kidneys is growing. A promising area of pathogenetic prevention and treatment of kidney disease is an interdisciplinary approach, whereat the adipokine imbalance is of particular interest. Adipose tissue and its messengers, adipokines, are known to be highly associated with kidney disease. Adipocytes are metabolically active cells, producing the signaling lipids, metabolites and protein factors, i.e. adipokines. The interaction of adipose tissue with the kidney is called the adipose kidney axis, being important for the normal functioning of the body, as well as its response to an injury. It has a strong therapeutic potential in respect of the growing rates of chronic kidney disease. Adipocyte hypertrophy is often accompanied by the development of tissue fibrosis, hypoxia, and secretion of pro−inflammatory cytokines (such as tumor necrosis factor or interleukin, which triggers the cell inflammation). Dysfunction of adipose tissue contributes to the development of cardiovascular disease at the local and systemic levels. Thus, for the early diagnosis of chronic kidney disease into the diagnostic program, in addition to the generally accepted indices, the determination of adipokines: for example, serum leptin, adiponectin, omentin, visfatin, microalbuminuria, blood lipid spectrum, intrarenal and functional status of the kidneys with the assessment of functional renal reserve is recommended to be included. Early detection of the disease, new approaches to its diagnosis and treatment can help in reducing the risk of a high incidence and mortality from renal disease. Key words: chronic kidney disease, nephropathy, adipokines, leptin, resistin, adiponectin, visfatin, omentin.

scholarly journals Role of specialized pro-resolving lipid mediators in pulmonary inflammation diseases: mechanisms and development

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ailin Yang ◽  
Yanjun Wu ◽  
Ganggang Yu ◽  
Haoyan Wang
Keyword(s):  
Immune Cells ◽  
Immune Modulation ◽  
Respiratory Diseases ◽  
Preventive Measures ◽  
Pulmonary Inflammation ◽  
Lipid Mediators ◽  
Pulmonary Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

AbstractInflammation is an essential mechanism of various diseases. The development and resolution of inflammation are complex immune-modulation processes which induce the involvement of various types of immune cells. Specialized pro-resolving lipid mediators (SPMs) have been demonstrated to be signaling molecules in inflammation. SPMs are involved in the pathophysiology of different diseases, especially respiratory diseases, including asthma, pneumonia, and chronic obstructive pulmonary disease. All of these diseases are related to the inflammatory response and its persistence. Therefore, a deeper understanding of the mechanisms and development of inflammation in respiratory disease, and the roles of the SPM family in the resolution process, might be useful in the quest for novel therapies and preventive measures for pulmonary diseases.

scholarly journals Histone Methylation Related Therapeutic Challenge in Cardiovascular Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Yang Yang ◽  
Ying Luan ◽  
Rui-Xia Yuan ◽  
Yi Luan
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Histone Modifications ◽  
Histone Methylation ◽  
Therapeutic Potential ◽  
Vascular Inflammation ◽  
Cellular Functions ◽  
Inflammatory Reactions ◽  
High Prevalence

The epidemic of cardiovascular diseases (CVDs) is predicted to spread rapidly in advanced countries accompanied by the high prevalence of risk factors. In terms of pathogenesis, the pathophysiology of CVDs is featured by multiple disorders, including vascular inflammation accompanied by simultaneously perturbed pathways, such as cell death and acute/chronic inflammatory reactions. Epigenetic alteration is involved in the regulation of genome stabilization and cellular homeostasis. The association between CVD progression and histone modifications is widely known. Among the histone modifications, histone methylation is a reversible process involved in the development and homeostasis of the cardiovascular system. Abnormal methylation can promote CVD progression. This review discusses histone methylation and the enzymes involved in the cardiovascular system and determine the effects of histone methyltransferases and demethylases on the pathogenesis of CVDs. We will further demonstrate key proteins mediated by histone methylation in blood vessels and review histone methylation-mediated cardiomyocytes and cellular functions and pathways in CVDs. Finally, we will summarize the role of inhibitors of histone methylation and demethylation in CVDs and analyze their therapeutic potential, based on previous studies.

scholarly journals The Protective Effects of IL-31RA Deficiency During Bleomycin-Induced Pulmonary Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Dan J. K. Yombo ◽  
Varshini Odayar ◽  
Nishant Gupta ◽  
Anil G. Jegga ◽  
Satish K. Madala
Keyword(s):  
T Cells ◽  
Lung Function ◽  
Pulmonary Fibrosis ◽  
Gene Networks ◽  
Therapeutic Potential ◽  
Pulmonary Inflammation ◽  
Protective Effects ◽  
Collagen Deposition ◽  
Lung Function Decline

Idiopathic Pulmonary Fibrosis (IPF) is a severe fibrotic lung disease characterized by excessive collagen deposition and progressive decline in lung function. Th2 T cell-derived cytokines including IL-4 and IL-13 have been shown to contribute to inflammation and fibrotic remodeling in multiple tissues. Interleukin-31 (IL-31) is a newly identified cytokine that is predominantly produced by CD4 Th2 T cells, but its signaling receptor IL-31RA is primarily expressed by non-hematopoietic cells. However, the potential role of the IL-31-IL31RA axis in pulmonary inflammation and fibrosis has remained largely unknown. To determine the role of IL-31RA deficiency in pulmonary fibrosis, wildtype, and IL-31RA knockout mice were treated with bleomycin and measured changes in collagen deposition and lung function. Notably, the loss of IL-31 signaling attenuated collagen deposition and lung function decline during bleomycin-induced pulmonary fibrosis. The total lung transcriptome analysis showed a significant reduction in fibrosis-associated gene transcripts including extracellular matrix and epithelial cell-associated gene networks. Furthermore, the lungs of human IPF showed an elevated expression of IL-31 when compared to healthy subjects. In support, the percentage of IL-31 producing CD4+ T cells was greater in the lungs and PBMCs from IPF patients compared to healthy controls. Our findings suggest a pathogenic role for IL-31/IL-31RA signaling during bleomycin-induced pulmonary fibrosis. Thus, therapeutic targeting the IL-31-IL-31RA axis may prevent collagen deposition, improve lung function, and have therapeutic potential in pulmonary fibrosis.

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