scholarly journals Role of melatonin in the angiogenesis potential; highlights on the cardiovascular disease

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Afshin Rahbarghazi ◽  
Marefat Siahkouhian ◽  
Reza Rahbarghazi ◽  
Mahdi Ahmadi ◽  
Lotfali Bolboli ◽  
...  

AbstractMelatonin possesses multi-organ and pleiotropic effects with potency to control angiogenesis at both molecular and cellular levels. To date, many efforts have been made to control and regulate the dynamic of angiogenesis modulators in a different milieu. The term angiogenesis or neovascularization refers to the development of de novo vascular buds from the pre-existing blood vessels. This phenomenon is tightly dependent on the balance between the pro- and anti-angiogenesis factors which alters the functional behavior of vascular cells. The promotion of angiogenesis is thought to be an effective strategy to accelerate the healing process of ischemic changes such as infarcted myocardium. Of note, most of the previous studies have focused on the anti-angiogenesis capacity of melatonin in the tumor niche. To the best of our knowledge, few experiments highlighted the melatonin angiogenesis potential and specific regulatory mechanisms in the cardiovascular system. Here, we aimed to summarize some previous experiments related to the application of melatonin in cardiovascular diseases such as ischemic injury and hypertension by focusing on the regulatory mechanisms.

2013 ◽  
Vol 126 (3) ◽  
pp. 183-194 ◽  
Author(s):  
Kasey C. Vickers ◽  
Kerry-Anne Rye ◽  
Fatiha Tabet

Physiological and pathological roles for small non-encoding miRNAs (microRNAs) in the cardiovascular system have recently emerged and are now widely studied. The discovery of widespread functions of miRNAs has increased the complexity of gene-regulatory processes and networks in both the cardiovascular system and cardiovascular diseases. Indeed, it has recently been shown that miRNAs are implicated in the regulation of many of the steps leading to the development of cardiovascular disease. These findings represent novel aspects in miRNA biology and, therefore, our understanding of the role of these miRNAs during the pathogenesis of cardiovascular disease is critical for the development of novel therapies and diagnostic interventions. The present review will focus on understanding how miRNAs are involved in the onset and development of cardiovascular diseases.


Author(s):  
Hongyang Shu ◽  
Yizhong Peng ◽  
Weijian Hang ◽  
Ning Zhou ◽  
Dao Wen Wang

Valosin-containing protein (VCP/p97) is a member of the conserved type II AAA+ (ATPases associated with diverse cellular activities) family of proteins with multiple biological functions, especially in protein homeostasis. Mutations in VCP/p97 are reportedly related to unique autosomal dominant diseases, which may worsen cardiac function. Although the structure of VCP/p97 has been clearly characterized, with reports of high abundance in the heart, research focusing on the molecular mechanisms underpinning the roles of VCP/p97 in the cardiovascular system has been recently undertaken over the past decades. Recent studies have shown that VCP/p97 deficiency affects myocardial fibers and induces heart failure, while overexpression of VCP/p97 eliminates ischemia/reperfusion injury and relieves pathological cardiac hypertrophy caused by cardiac pressure overload, which is related to changes in the mitochondria and calcium overload. However, certain studies have drawn opposing conclusions, including the mitigation of ischemia/reperfusion injury via inhibition of VCP/p97 ATPase activity. Nevertheless, these emerging studies shed light on the role of VCP/p97 and its therapeutic potential in cardiovascular diseases. In other words, VCP/p97 may be involved in the development of cardiovascular disease, and is anticipated to be a new therapeutic target. This review summarizes current findings regarding VCP/p97 in the cardiovascular system for the first time, and discusses the role of VCP/p97 in cardiovascular disease.


BMJ Open ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. e032633 ◽  
Author(s):  
Kuo-Liong Chien ◽  
Ting-Yu Lin ◽  
Chen-Yang Hsu ◽  
Chang-Chuan Chan ◽  
Tony Hsiu-Hsi Chen ◽  
...  

ObjectivesThe role of faecal haemoglobin as a colorectal cancer screening tool has been demonstrated. However, the association between the faecal haemoglobin concentration and the risk of cardiovascular disease events and deaths is still unclear.DesignCohort study design.SettingPopulation-based organised integrated service screening in Keelung City, TaiwanParticipantsA total of 33 355 healthy individuals aged over 40 years who were free of cardiovascular disease at study entry were followed up.Main outcomes and measuresNewly diagnosed cardiovascular disease events and deaths.ResultsAfter a median follow-up of 2.39 years, a total of 2768 participants developed cardiovascular events, and after a median follow-up of 8.43 years, 317 cases of cardiovascular deaths occurred. The risk of cardiovascular disease increased with baseline faecal haemoglobin in a dose–response manner, yielding a significant elevated risk of cardiovascular disease in parallel with the incremental concentration of faecal haemoglobin (adjusted HRs=1.04, 1.10, 1.40 and 1.23 for faecal haemoglobin concentrations of 1–19, 20–49, 50–99 and ≥100 ng/mL, trend test, p<0.0001, as compared with the reference group with undetectable faecal haemoglobin concentrations). A similar pattern was observed for the risk of cardiovascular disease deaths. In addition, the faecal haemoglobin improved the prediction performance of the model for the risk of cardiovascular diseases; the integrated discrimination improvement was 0.3% (p<0.001) for cardiovascular events and 0.1% (p=0.020) for cardiovascular deaths.ConclusionsOur data support that faecal haemoglobin concentrations may be associated with the risk of cardiovascular diseases. The biological mechanisms underlying the role of faecal haemoglobin as health outcomes should be investigated.


2016 ◽  
Vol 94 (7) ◽  
pp. 497-503 ◽  
Author(s):  
A. F. Verbovoy ◽  
Lyudmila A. Sharonova ◽  
O. V. Kosareva ◽  
N. I. Verbovaya ◽  
Yu. A. Dolgikh

The article presents data on the relationship between thyroid dysfunction and cardiovascular diseases. The role of dyslipidemia, adipokines (adiponectin, leptin, resistin), C-reactive protein, deficiency of vitamin D3 in the development of cardiovascular disease in hypothyroidism is discussed. The article describes characteristics of myocardial remodeling, its dysfunction and their correlation with risk factors of cardiovascular diseases in patients with hypothyroidism.


2014 ◽  
Vol 25 (12) ◽  
pp. 1867-1876 ◽  
Author(s):  
Emily M. Vaughan ◽  
Jae-Sung You ◽  
Hoi-Ying Elsie Yu ◽  
Amber Lasek ◽  
Nicolas Vitale ◽  
...  

After damage, cells reseal their plasma membrane and repair the underlying cortical cytoskeleton. Although many different proteins have been implicated in cell repair, the potential role of specific lipids has not been explored. Here we report that cell damage elicits rapid formation of spatially organized lipid domains around the damage site, with different lipids concentrated in different domains as a result of both de novo synthesis and transport. One of these lipids—diacylglycerol (DAG)—rapidly accumulates in a broad domain that overlaps the zones of active Rho and Cdc42, GTPases that regulate repair of the cortical cytoskeleton. Formation of the DAG domain is required for Cdc42 and Rho activation and healing. Two DAG targets, protein kinase C (PKC) β and η, are recruited to cell wounds and play mutually antagonistic roles in the healing process: PKCβ participates in Rho and Cdc42 activation, whereas PKCη inhibits Rho and Cdc42 activation. The results reveal an unexpected diversity in subcellular lipid domains and the importance of such domains for a basic cellular process.


2020 ◽  
pp. 21-31 ◽  
Author(s):  
O. KITTNAR

The annual incidence of cardiovascular diseases is age-dependently increasing both in men and women, however, the prevalence is higher in men until midlife. The higher incidence of cardiovascular disease in men than in women of similar age, and the menopause-associated increase in cardiovascular disease in women, has led to speculation that gender-related differences in sex hormones might have a key role in the development and evolution of cardiovascular disease. There are several suggested pathways in which gender and sex hormones can affect human cardiovascular system to produce original sexually different pathophysiology between women and men. Sex steroid hormones and their receptors are critical determinants of cardiovascular gender differences. Also arterial blood pressure is typically lower in women than in men what could be explained particularly by greater synthesis of nitric oxide (NO) in women. Female cardiomyocytes have a greater survival advantage when challenged with oxidative stress, suggesting that female hormones may play an important role in antioxidative protection of myocardium. It was also demonstrated in animal models that combination of XX chromosomes versus an XY chromosomes enhances sex differences in higher HDL cholesterol. Women were found to have reduced sympathetic activity (reflected by lower total peripheral resistance) and pulmonary artery pressure and enhanced parasympathetic activity relative to men. Similarly, men were found to have higher plasma norepinephrine levels than women. Regarding differences between the sexes in electrophysiology of the heart, two principle mechanisms have been proposed to explain them: hormonal effects on the expression or function of ion channels or, conversely, differences in autonomic tone. To improve diagnosis and treatment of cardiovascular diseases, greater focus on understanding the molecular and cellular physiology of the sex steroid hormones and their receptors in the cardiovascular system will be required.


2021 ◽  
Author(s):  
Aiman Hilmi Asaduddin ◽  
Shafira Yasmine Anshari ◽  
Agni Shalha Ali ◽  
Ardhia Fefrine Indarta ◽  
Muhammad Adrianes Bachnas ◽  
...  

Abstract Background There are two central dogmas between the pathophysiology of preeclampsia, the placental origin and the extra-placental origin. Recent findings found that women with a history of preeclampsia are at higher risk of cardiovascular disease and death because of cardiovascular disease. This finding leads to the extra-placental origin. During normal pregnancy, the maternal cardiovascular system undergoes modification. However, hemodynamic and vascular modification are disrupted in women who develop preeclampsia. NT-proBNP is a biomarker that indicates the disruption of the cardiovascular system and can predict the complication of preeclampsia. Based on that information, we would like to investigate the roles of NT-proBNP plasma levels in predicting maternal and fetal complications of preeclampsia women. Besides, we also investigate the roles of NT-proBNP plasma levels in predicting the severity and onset of preeclampsia women and the sensitivity and specificity of NT-proBNP plasma levels in preeclamptic women.MethodsWe designed and registered a study protocol for a systematic review. This study aims to investigate the roles of NT-proBNP plasma levels in predicting maternal and fetal complications of preeclampsia women. The Cochrane Handbook for Systematic Reviews of Diagnostic Test Accuracy was used to structure our methodological approach and the Preferred Reporting Items for a Systematic Review and Meta-Analysis Protocols guidelines in reporting the findings of this review. We will search literature in Hinari, Cochrane Library, ScienceDirect, and Scopus database. Then, we will search the grey literature in OCLC’s OAISTER. Randomized controlled trials and observational studies will be included in the analysis. Three reviewers will independently screen articles, extract data, and evaluate for quality and bias using Newcastle-Ottawa Scale. Studies were included according to the following procedures: (1) Identification, Duplication of articles and non-original research articles will be excluded; (2) Title and Abstract Screening, RCT and observational studies and focused on NT-proBNP levels in preeclampsia; (3) Full-text availability; and (4) Full-text screening based on PICO criteria. Each outcome is synthesized by a qualitative or narrative approach. The results will be divided into certain points, namely (a) Selection of the studies, (b) Characteristics of the Eligible Studies, (c) Data Extraction of the Eligible Studies, and (d) Risk of Bias Analysis Results.Discussion A systematic review of the role of NT-proBNP as predicting biomarkers for preeclampsia complications will be conducted. This study can help predict the severity, onset, and complication of a pregnant woman with preeclampsia.


2020 ◽  
Vol 21 (14) ◽  
pp. 5005 ◽  
Author(s):  
Bruno Bragança ◽  
Paulo Correia-de-Sá

Adenosine triphosphate (ATP) is a primordial versatile autacoid that changes its role from an intracellular energy saver to a signaling molecule once released to the extracellular milieu. Extracellular ATP and its adenosine metabolite are the main activators of the P2 and P1 purinoceptor families, respectively. Mounting evidence suggests that the ionotropic P2X4 receptor (P2X4R) plays pivotal roles in the regulation of the cardiovascular system, yet further therapeutic advances have been hampered by the lack of selective P2X4R agonists. In this review, we provide the state of the art of the P2X4R activity in the cardiovascular system. We also discuss the role of P2X4R activation in kidney and lungs vis a vis their interplay to control cardiovascular functions and dysfunctions, including putative adverse effects emerging from P2X4R activation. Gathering this information may prompt further development of selective P2X4R agonists and its translation to the clinical practice.


2017 ◽  
Vol 12 (02) ◽  
pp. 1 ◽  
Author(s):  
Carolyn M Webb ◽  
Peter Collins ◽  
◽  

Cardiovascular disease (CVD) is the most prevalent non-communicable cause of death worldwide. Testosterone is a sex hormone that is predominant in males but also occurs in lower concentrations in females. It has effects directly on the blood vessels of the cardiovascular system and on the heart, as well as effects on risk factors for CVD. Serum testosterone concentrations are known to decrease with age and reduced testosterone levels are linked to premature coronary artery disease, unfavourable effects on CVD risk factors and increased risk of cardiovascular mortality independent of age. A significant number of men with heart failure demonstrate reduced serum testosterone concentrations and there is early evidence suggesting that low testosterone levels affect cardiac repolarisation. Any association between endogenous testosterone concentrations and CVD in women has yet to be established. Testosterone replacement is used to treat men with hypogonadism but also has cardiovascular effects. This review will present the current evidence, expert opinion and controversies around the role of testosterone in the pathophysiology of CVD and surrounding the use of testosterone treatment and its effects on the cardiovascular system and CVD.


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