scholarly journals Non-Coding RNAs in Cardiac Aging

2015 ◽  
Vol 36 (5) ◽  
pp. 1679-1687 ◽  
Author(s):  
Hui Wang ◽  
Yihua Bei ◽  
Jing Shi ◽  
Junjie Xiao ◽  
Xiangqing Kong

Aging has a remarkable impact on the function of the heart, and is independently associated with increased risk for cardiovascular diseases. Cardiac aging is an intrinsic physiological process that results in impaired cardiac function, along with lots of cellular and molecular changes. Non-coding RNAs include small transcripts, such as microRNAs and a wide range of long non-coding RNAs (lncRNAs). Emerging evidence has revealed that non-coding RNAs acted as powerful and dynamic modifiers of cardiac aging. This review aims to provide a general overview of non-coding RNAs implicated in cardiac aging, and the underlying mechanisms involved in maintaining homeo-stasis and retarding aging.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
W Wang ◽  
Y Zhou ◽  
J Xu ◽  
S Zhang ◽  
Y Meng

Abstract Background The elevated plasma homocysteine (Hcy) level can lead to severe cardiovascular injuries, which participates in the progression of atherosclerosis, heart failure and so on. Except cardiovascular diseases, accumulated researches further revealed that hyperhomocystenemia (HHcy) can also induce aging-related diseases, including Alzheimer's disease, Parkinson's disease, diabetic cardiomyopathy, etc. Though some researches had revealed that Hcy stimulation would lead to endothelial cells senescence, whether cardiac aging could be induced by HHcy still remain unknown. Purpose This study aimed to reveal whether HHcy can induce cardiac aging and the underlying mechanisms. Methods SD rats were utilized to establish HHcy rat model and natural aging rat model. The cardiac function were determined by Echocardiography. Transmission electron microscope were used to detect mitochondria injuries of myocardium. 18F-FDG PET/CT was used to detect the state of glucose metabolism in myocardial cells. Agilent mRNA Array was used to detect possible altered pathways in myocardium of HHcy rats. The autophagy level was determined by detection of both autophagy-related proteins expressions with Western Blot and autophagic flux with mRFP-GFP-LC3. Results HHcy rats showed overall aging phenotypes, which were consistent with natural aging rats. The impaired cardiac function and severely injured myocardium morphology were observed in HHcy rats. Aging-related markers were increased significantly in HHcy rats and Hcy-treated cells, presented as increased p16, p21 and p53 expressions and increased senescence-associated beta-galactosidase (SA-β-gal) activity. Mitochondria dysfunction and morphology injuries were also detected in HHcy rats. Moreover, decreased serum Beclin-1 level was tested in CHD patients with HHcy. The decreased autophagy level was further verified in HHcy rats and Hcy-treated cells. Furthermore, the over-expression of Atg5 could attenuate Hcy induced cellular senescence. Conclusion HHcy can reduce autophagy level, which leading to severe mitochondria injuries, and resulted in cardiac aging eventually. Acknowledgement/Funding Natural Science Foundation of China (81671382,91839107)


2020 ◽  
Vol 90 (2) ◽  
Author(s):  
Sara Paris ◽  
Luigi Tarantini ◽  
Alessandro Navazio ◽  
Pompilio Faggiano

Even if cancer and cardiovascular diseases are considered two distinct diseases, an intricate interconnection between these conditions has been established. Increased risk of malignancy has been identified in patients with cardiovascular disease, as well as a greater propensity to the development of cardiovascular diseases has been observed in patients with cancer. The development of cardiotoxicity following exposure to certain anticancer drugs only partially explains this relationship. Shared risk factors and common pathogenic mechanisms suggest the existence of a common biology and a complex interplay between these two conditions. Due to improving longevity and therapeutic advances, the number of patients affected or potentially at risk of developing these two diseases is constantly increasing and currently, several drugs against cancer from anthracyclines to checkpoint inhibitors, can also cause a wide range of unexpected cardiovascular side effects. Management of these issues in clinical practice is an emerging challenge for cardiologists and oncologists, and led to the development of a new dedicated discipline called cardio-oncology. Surveillance and prevention strategies as well as interventions to reduce cardiovascular risk and prevent cardiotoxicities are the primary objectives of cardio-oncology. In this review, we explore the etiopathogenesis common to cardiovascular disease and cancer and the complex interplay between them. We also report the main characteristics of the drugs responsible for cardiotoxicity, highlighting the available strategies for optimal patient management based on a multidisciplinary approach in the cardio-oncology setting.


2021 ◽  
Author(s):  
Hongfei Ge ◽  
Gongxin Liu ◽  
Tracy M. Yamawaki ◽  
Caroline Tao ◽  
Shawn T. Alexander ◽  
...  

Abstract Heart failure (HF) and cardiac arrhythmias share overlapping pathological mechanisms that act cooperatively to accelerate disease pathogenesis. Cardiac fibrosis is associated with both pathological conditions. Our previous work identified a link between phytosterol accumulation and cardiac injury in a mouse model of phytosterolemia, a rare disorder characterized by elevated circulating phytosterols and increased cardiovascular disease risk. Here, we uncover a previously unknown pathological link between phytosterols and cardiac arrhythmias in the same animal model. Phytosterolemia resulted in inflammatory pathway induction, premature ventricular contractions (PVC) and ventricular tachycardia (VT). Both pharmacological and genetic inhibition of phytosterol absorption prevented the induction of both pathways. Inhibition of phytosterol absorption reduced inflammation and cardiac fibrosis, improved cardiac function, reduced the incidence of arrhythmias and increased survival in a mouse model of phytosterolemia. Collectively, this work identified a pathological mechanism whereby elevated phytosterols result in inflammation and cardiac fibrosis leading to impaired cardiac function, arrhythmias and sudden death. These phytosterolemia-associated comorbidities provide novel insight into the underlying pathophysiological mechanism that predispose these patients to increased risk of sudden cardiac death.


2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Adeleh Shirangi ◽  
Alex Xiao ◽  
Emmanuel Ongee ◽  
Ivana Ivánová ◽  
Ashraf Dewan ◽  
...  

Abstract Background Understanding the health effects of smoke from landscape fires (LFs), including wildfires and prescribed burns, is limited due to lack of adequate smoke exposure measures. Methods We used the reported LFs to determine smoke plume shapes from satellite images. Daily remotely sensed fire radiative power, aerosol optical depth, smoke plumes, fire danger rating, venting index and previous day PM 2.5 were then used to estimate smoke-related particulate matter 2.5 (PM2.5). A population based time series design was used to assess associations between smoke-related PM2.5 and selected adverse health outcomes such as hospital admissions, emergency department visits and ambulance callouts. Results We found a significant dose-response relationship between increased smoke-related PM2.5 concentration and 1% to 5% increase for total emergency department attendances and total hospital admissions on the same day and the lag effects of 3 days where the PM2.5 was at medium level (95-98th percentile) and high level ( > =99th percentile) compared to the low level (<95th percentile). There was also 1% to 25% increased risk for individuals who were exposed to high level LF smoke with selected respiratory and cardiovascular diseases in selected health care utilisations. Conclusions Exposure to LF smoke at a high level was spatio-temporally associated with a wide range of adverse respiratory and cardiovascular diseases in selected health care utilisations. Key messages


Author(s):  
Vivette Glover

Many independent prospective studies show maternal stress, anxiety, or depression during pregnancy poses an increased risk for her child to have a wide range of adverse outcomes including emotional problems, ADHD or conduct disorder, or impaired cognitive development. Several studies have shown that these adverse outcomes are independent of possible confounding factors, such as postpartum anxiety and depression. Most children are not affected, and those who are can be affected in different ways, probably due to different genetic vulnerabilities and the quality of postpartum care. An evolutionary explanation for the observed changes is proposed. Underlying mechanisms are just starting to be understood: altered function of the placenta, allowing more of the stress hormone cortisol to pass through to the fetus, may well be important, as may epigenetic changes. The implications are that improved emotional care of pregnant women should improve outcomes for their children to a clinically significant degree.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Koichiro Matsumura ◽  
Tetsuro Sugiura

Abstract A high incidence of left ventricular diastolic dysfunction and increased risk of cardiovascular events have been reported in patients with diabetes mellitus. Sodium glucose cotransporter 2 (SGLT2) inhibitors selectively inhibit kidney glucose and sodium reabsorption, and cardiovascular benefits of SGLT2 inhibitors beyond other antidiabetic drugs have been reported in type 2 diabetes mellitus (T2DM) clinical trials. However, underlying mechanisms contributing to the improvement of cardiovascular outcomes have not been clearly identified. In this review, likely mechanisms of SGLT2 inhibitors contributing to a favorable cardiovascular outcomes are discussed based on experimental and clinical studies on cardiac function.


Pathologia ◽  
2021 ◽  
Vol 18 (2) ◽  
pp. 229-242
Author(s):  
M. P. Kopytsia ◽  
Yu. V. Rodionova ◽  
N. V. Tytarenko ◽  
I. M. Kutia ◽  
Ya. V. Нilоva

Myeloperoxidase is one of the key enzymes involved in oxidative stress and inflammation. Its elevated levels are determined in a wide range of both acute and chronic forms of cardiovascular diseases. The inflammation results in the release of the enzyme from the white blood cells to form products such as hypochlorous acid, which in turn can have a negative effect on the target proteins. Inconsistent evidence on the predictive role of this biomarker in diseases of the circulatory system generates scientific interest and provokes further research in this direction. The aim of this review is to analyze the scientific literature data on myeloperoxidase as a possible clinical use for the diagnosis and risk stratification of patients with саrdiovascular diseases. Materials and methods. Searching and generalization of data from leading specialized sources, which are indexed by scientific databases PubMed, SCOPUS, Web of Science. Results. The results of the studies indicate that myeloperoxidase is actively involved in the pathophysiology of cardiovascular diseases through participation in oxidative stress and inflammation, excessive production of proatherogenic lipoproteins, changes in nitric oxide activity, endothelial dysfunction, and due to the effect on the instability of atherosclerotic plaques. In patients with cardiovascular diseases, including ischemic heart disease, the concentration of the indicated protein is increased and is often associated with a poor prognosis, including an increased risk of mortality. Myeloperoxidase metabolites are often the factors that contribute to cell damage under conditions of ischemia. The review also considers the relationship of the enzyme with the development of restenosis and the effectiveness of revascularization after percutaneous coronary intervention. Conclusions. The presented data mainly define myeloperoxidase as a significant marker for predicting long-term follow-up results and the development of serious adverse cardiovascular events, mortality in patients with cardiovascular disease. At the same time, despite the great achievements in disclosing the complex effects of myeloperoxidase, inconsistency in the available results is noteworthy. This controversy necessitates further research to elucidate and reveal the full clinical potential of myeloperoxidase in patients with cardiovascular pathology.


Author(s):  
Andrey V. Melentyev

Introduction. One of the leading causes of occupational health loss, especially in mining and machine-building enterprises, is the combined impact of industrial noise and vibration. The wide prevalence of cardiovascular diseases is one of the most important medical and social problems, due to persistent disability and high mortality, bringing prevention of health disorders to the first place as the basis for preserving labor longevity. The aim of study is to identify the main approaches aimed at preventing health problems in workers who come into contact with vibration and noise at mining and machine-building enterprises. Materials and methods. A survey and survey of 296 industrial workers was conducted. Group 1 (160 people) included men who were exposed to noise and vibration factors above the maximum permissible levels, group 2 consisted of 136 men who did not have direct contact with noise and vibration generating equipment. When conducting an in-depth laboratory and instrumental examination in a hospital setting, all workers additionally calculated the level of cardiovascular risk on the SCORE scale. Statistical analysis was performed using the software package "Statistica 6.0". Results. It is determined that the priority adverse factors of the working environment in production are noise and vibration. It has been shown that individuals who come into contact with these factors are more likely to detect violations of lipid metabolism and endothelial function, have a higher average heart rate and systolic blood pressure, and have an increased risk of developing cardiovascular diseases. Conclusions. Taking into account the obtained results of the proposed diagnostic approaches aimed at the prevention of health disorders among workers of industrial enterprises. If employees are found to have an increased cardiovascular risk, it is necessary to conduct a more in-depth examination and timely medical and preventive measures.


The prevalence of heart failure is markedly increased in individuals with diabetes mellitus. Numerous observational studies suggest that this increased risk for heart failure can be attributed to exacerbated vascular complications and the presence of increased risk factors in diabetic subjects. In addition, experimental studies revealed the presence of a number of distinct molecular alterations in the myocardium that occur independently of vascular disease and hypertension. Many of these molecular alterations are similarly observed in failing hearts of nondiabetic patients and have thus been proposed to contribute to the increased risk for heart failure in diabetes. The interest in understanding the underlying mechanisms of impaired cardio- vascular outcomes in diabetic individuals has much increased since the demonstration of cardioprotective effects of SGLT-2 inhibitors and GLP-1 receptor agonists in recent clinical trials. The current review therefore summarizes the distinct mechanisms that have been proposed to increase the risk for heart failure in diabetes mellitus.


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