scholarly journals Regulation of Mitochondrial Dynamics by Aerobic Exercise in Cardiovascular Diseases

2022 ◽  
Vol 8 ◽  
Author(s):  
Changping Gu ◽  
Jie Yan ◽  
Liang Zhao ◽  
Guanghan Wu ◽  
Yue-lan Wang
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Aerobic Exercise ◽  
Mitochondrial Function ◽  
Cardiovascular Health ◽  
Mitochondrial Dynamics ◽  
Pharmaceutical Intervention ◽  
Prevention And Treatment ◽  
And Function ◽  
Cvd Mortality

Mitochondrial dynamics, including continuous biogenesis, fusion, fission, and autophagy, are crucial to maintain mitochondrial integrity, distribution, size, and function, and play an important role in cardiovascular homeostasis. Cardiovascular health improves with aerobic exercise, a well-recognized non-pharmaceutical intervention for both healthy and ill individuals that reduces overall cardiovascular disease (CVD) mortality. Increasing evidence shows that aerobic exercise can effectively regulate the coordinated circulation of mitochondrial dynamics, thus inhibiting CVD development. This review aims to illustrate the benefits of aerobic exercise in prevention and treatment of cardiovascular disease by modulating mitochondrial function.

scholarly journals Elucidating the Relationship Between Insomnia, Sex, and Cardiovascular Disease

2020 ◽  
Vol 4 ◽  
pp. 247028972098001
Author(s):  
Rebecca Leeds ◽  
Ari Shechter ◽  
Carmela Alcantara ◽  
Brooke Aggarwal ◽  
John Usseglio ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Sex Differences ◽  
Cardiovascular Health ◽  
Future Research ◽  
Sex And Gender ◽  
Men And Women ◽  
Sex Research ◽  
And Gender ◽  
The Relationship ◽  
Cvd Mortality

Sex differences in cardiovascular disease (CVD) mortality have been attributed to differences in pathophysiology between men and women and to disparities in CVD management that disproportionately affect women compared to men. Similarly, there has been investigation of differences in the prevalence and presentation of insomnia attributable to sex. Few studies have examined how sex and insomnia interact to influence CVD outcomes, however. In this review, we summarize the literature on sex-specific differences in the prevalence and presentation of insomnia as well as existing research regarding the relationship between insomnia and CVD outcomes as it pertains to sex. Research to date indicate that women are more likely to have insomnia than men, and there appear to be differential associations in the relation between insomnia and CVD by sex. We posit potential mechanisms of the relationship between sex, insomnia and CVD, discuss gaps in the existing literature, and provide commentary on future research needed in this area. Unraveling the complex relations between sex, insomnia, and CVD may help to explain sex-specific differences in CVD, and identify sex-specific strategies for promotion of cardiovascular health. Throughout this review, terms “men” and “women” are used as they are in the source literature, which does not differentiate between sex and gender. The implications of this are also discussed.

P5994Role of BGP-15 treatment in hypertensive heart failure progression and mitochondrial protection

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Horvath ◽  
L Deres ◽  
K Ordog ◽  
K Bruszt ◽  
B Sumegi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mitochondrial Function ◽  
Cardiac Remodeling ◽  
In Vitro Model ◽  
Mitochondrial Dynamics ◽  
Treated Group ◽  
Mitochondrial Structure ◽  
Vitro Model ◽  
And Function

Abstract Introduction The deterioration of mitochondrial quality control greatly contributes to the hypertension induced cardiac remodeling and progression of heart failure. Our previous in vitro results demonstrated the mitochondrial protective effect of antioxidant BGP-15 compound in the presence of cellular stress. Purpose In our recent study we investigated the effect of BGP-15 on cardiac remodeling in spontaneously hypertensive rats (SHR) with manifested heart failure and on mitochondrial dynamics and function in cell culture model. Methods 15-month-old male SHR received 25 mg/kg/day BGP-15 (SHR-B) or placebo (SHR-C) for 18 weeks. Age matched Wistar rats (WKY) were used as normotensive control. The heart function was monitored by echocardiography. Histological preparations were made from cardiac tissue. Neonatal rat cardiomyocytes (NRCMs) were used as in vitro model. 150 μM H2O2 stress and 50 μM BGP-15 treatment was applied. Mitochondrial network was stained with MitoTracker Red. Mitochondrial membrane potential was detected using JC-1 dye, while mitochondrial function was monitored by the Agilent Seahorse XFp, Cell Mito Stress Test. In both model the cellular levels of mitochondrial dynamics proteins were measured in Western blot. To study the ultrastructure we used electron microscopy in our in vivo and in vitro model. Results Left ventricular (LV) mass and LV wall thickness were increased significantly in SHR-C group compared to the initial values (p<0.05). These parameters were decreased considerably in the SHR-B group. Ejection fraction (EF%) decreased in both SHR group although this downturn was minimal because of the treatment. Chronic high blood pressure caused higher collagen deposition in SHR-C rats that was significantly diminished in the SHR-B group. Regarding the mitochondrial function decrease in the levels of fusion proteins OPA1 and MFN2 was observed in the SHR-C group. These differences were significantly reduced by BGP-15 treatment (p<0.05). Mitigation of the level of fission protein DRP1 was however reduced by BGP-15 (p<0.05). In our cellular model, we observed that the H2O2-induced mitochondrial fragmentation was decreased by BGP-15 treatment (p<0.05). BGP-15 treatment prevented mitochondrial membrane potential fall in H2O2 stress (p<0.05). There was no significant difference in basal respiration among groups by monitoring the mitochondrial function. The maximal respiration capacity and ATP production were significantly higher in the BGP-15 treated group in comparison to the stressed group (p<0.05). Conclusion BGP-15 treatment has beneficial effects on mitochondrial dynamics and structure by promoting fusion processes. It also supports the maintenance of mitochondrial function through the preservation of the mitochondrial structure. The mitigation of remodeling processes and the preserved EF in the treated group are results at least partly of the comprehensible effects of BGP-15 on mitochondrial structure and function. Acknowledgement/Funding GINOP-2.3.2-15-2016-00049; GINOP-2.3.2-15-2016-00048; GINOP-2.3.3-15-2016-00025

scholarly journals Plasticizers and Cardiovascular Health: Role of Adipose Tissue Dysfunction

2021 ◽  
Vol 11 ◽  
Author(s):  
Mikyla A. Callaghan ◽  
Samuel Alatorre-Hinojosa ◽  
Liam T. Connors ◽  
Radha D. Singh ◽  
Jennifer A. Thompson
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Adverse Effects ◽  
Cardiovascular Health ◽  
The United States ◽  
Current Evidence ◽  
Endocrine Disrupting ◽  
And Function

Since the 1950s, the production of plastics has increased 200-fold, reaching 360 million tonnes in 2019. Plasticizers, additives that modify the flexibility and rigidity of the product, are ingested as they migrate into food and beverages. Human exposure is continuous and widespread; between 75 and 97% of urine samples contain detectable levels of bisphenols and phthalates, the most common plasticizers. Concern over the toxicity of plasticizers arose in the late 1990s, largely focused around adverse developmental and reproductive effects. More recently, many studies have demonstrated that exposure to plasticizers increases the risk for obesity, type 2 diabetes, and cardiovascular disease (CVD). In the 2000s, many governments including Canada, the United States and European countries restricted the use of certain plasticizers in products targeted towards infants and children. Resultant consumer pressure motivated manufacturers to substitute plasticizers with analogues, which have been marketed as safe. However, data on the effects of these new substitutes are limited and data available to-date suggest that many exhibit similar properties to the chemicals they replaced. The adverse effects of plasticizers have largely been attributed to their endocrine disrupting properties, which modulate hormone signaling. Adipose tissue has been well-documented to be a target of the disrupting effects of both bisphenols and phthalates. Since adipose tissue function is a key determinant of cardiovascular health, adverse effects of plasticizers on adipocyte signaling and function may underlie their link to cardiovascular disease. Herein, we discuss the current evidence linking bisphenols and phthalates to obesity and CVD and consider how documented impacts of these plasticizers on adipocyte function may contribute to the development of CVD.

scholarly journals FUNDC1: A Promising Mitophagy Regulator at the Mitochondria-Associated Membrane for Cardiovascular Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Guoyong Li ◽  
Junli Li ◽  
Ruochen Shao ◽  
Jiahao Zhao ◽  
Mao Chen
Keyword(s):  
Cardiovascular Diseases ◽  
Ischemia Reperfusion Injury ◽  
Mitochondrial Dynamics ◽  
Ischemia Reperfusion ◽  
Septic Cardiomyopathy ◽  
Cellular Processes ◽  
Contact Sites ◽  
Promising Therapeutic Target ◽  
And Function ◽  
Cellular Organelles

Mitochondrial autophagy (or mitophagy) regulates the mitochondrial network and function to contribute to multiple cellular processes. The protective effect of homeostatic mitophagy in cardiovascular diseases (CVDs) has attracted increasing attention. FUN14 domain containing 1 (FUNDC1), an identified mitophagy receptor, plays an essential role in CVDs. Different expression levels of FUNDC1 and its phosphorylated state at different sites alleviate or exacerbate hypoxia and ischemia/reperfusion injury, cardiac hypertrophy, or metabolic damage through promotion or inhibition of mitophagy. In addition, FUNDC1 can be enriched at contact sites between mitochondria and the endoplasmic reticulum (ER), determining the formation of mitochondria-associated membranes (MAMs) that regulate cellular calcium (Ca2+) homeostasis and mitochondrial dynamics to prevent heart dysfunction. Moreover, FUNDC1 has also been involved in inflammatory cardiac diseases such as septic cardiomyopathy. In this review, we collect and summarize the evidence on the roles of FUNDC1 exclusively in various CVDs, describing its interactions with different cellular organelles, its involvement in multiple cellular processes, and its associated signaling pathways. FUNDC1 may become a promising therapeutic target for the prevention and management of various CVDs.

scholarly journals Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Ying Tan ◽  
Fengfan Xia ◽  
Lulan Li ◽  
Xiaojie Peng ◽  
Wenqian Liu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Dynamics ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
Regulatory Mechanisms ◽  
Septic Cardiomyopathy ◽  
Mitochondrial Dynamic ◽  
Dynamic Disorder ◽  
Molecular Features ◽  
And Function

Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease.

scholarly journals Altered mitochondrial dynamics and function in APOE4-expressing astrocytes

2020 ◽  
Vol 11 (7) ◽  
Author(s):  
Eran Schmukler ◽  
Shira Solomon ◽  
Shira Simonovitch ◽  
Yona Goldshmit ◽  
Eya Wolfson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Transgenic Mice ◽  
Mitochondrial Function ◽  
Mitochondrial Dynamics ◽  
Major Risk Factor ◽  
Sporadic Alzheimer’S Disease ◽  
Dynamics And Function ◽  
And Function

Abstract APOE4 is a major risk factor for sporadic Alzheimer’s disease; however, it is unclear how it exerts its pathological effects. Others and we have previously shown that autophagy is impaired in APOE4 compared to APOE3 astrocytes, and demonstrated differences in the expression of mitochondrial dynamics proteins in brains of APOE3 and APOE4 transgenic mice. Here, we investigated the effect of APOE4 expression on several aspects of mitochondrial function and network dynamics, including fusion, fission, and mitophagy, specifically in astrocytes. We found that APOE3 and APOE4 astrocytes differ in their mitochondrial dynamics, suggesting that the mitochondria of APOE4 astrocytes exhibit reduced fission and mitophagy. APOE4 astrocytes also show impaired mitochondrial function. Importantly, the autophagy inducer rapamycin enhanced mitophagy and improved mitochondrial functioning in APOE4 astrocytes. Collectively, the results demonstrate that APOE4 expression is associated with altered mitochondrial dynamics, which might lead to impaired mitochondrial function in astrocytes. This, in turn, may contribute to the pathological effects of APOE4 in Alzheimer’s disease.

Abstract 16562: Association of County-Level Social Vulnerability Index and Cardiovascular Disease in the United States, 1999-2018

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Quentin R Youmans ◽  
Megan E McCabe ◽  
Clyde W Yancy ◽  
Lucia Petito ◽  
Kiarri N Kershaw ◽  
...  
Keyword(s):  
United States ◽  
Cardiovascular Disease ◽  
Social Vulnerability ◽  
Cardiovascular Health ◽  
Vulnerability Index ◽  
The United States ◽  
County Level ◽  
Social Vulnerability Index ◽  
Cross Sectional ◽  
Cvd Mortality

Introduction: Social determinants of health are multi-dimensional and span various interrelated domains. In order to inform community-engaged clinical and policy efforts, we sought to examine the association between a national social vulnerability index (SVI) and age-adjusted mortality rate (AAMR) of CVD. Hypothesis: Higher county-level SVI or greater vulnerability will be associated with higher AAMR of CVD between 1999-2018 in the United States. Methods: In this serial, cross-sectional analysis, we queried CDC WONDER for age-adjusted mortality rates (AAMRs) per 100,000 population for cardiovascular disease (I00-78) at the county-level between 1999-2018. We quantified the association of county-level SVI and CVD AAMR using Spearman correlation coefficients and examined trends in CVD AAMR stratified by median SVI at the county-level. Finally, we performed geospatial county-level analysis stratified by combined median SVI and CVD AAMR (high/high, high/low, low/high, and low/low). Results: We included data from 2766 counties (representing 95% of counties in the US) with median SVI 0.53 (IQR 0.28, 0.76). Overall SVI and the household and socioeconomic subcomponents were strongly correlated with 2018 CVD AAMR (0.47, 0.50, and 0.56, respectively with p<0.001 for all). CVD mortality declined between 1999-2011 and was stagnant between 2011-2018 with similar patterns in high and low SVI counties (FIGURE). Counties with high SVI and CVD AAMR were clustered in the South and Midwest (n=977, 35%). Conclusion: County-level social vulnerability is associated with higher CVD mortality. High SVI and CVD AAMR coexist in more than 1 in 3 US counties and have persisted over the past 2 decades. Identifying counties that are disproportionately vulnerable may inform targeted and community-based strategies to equitably improve cardiovascular health across the country.

scholarly journals The E3 ligase MARCH5 is a PPARγ target gene that regulates mitochondria and metabolism in adipocytes

2019 ◽  
Vol 316 (2) ◽  
pp. E293-E304 ◽  
Author(s):  
Simon T. Bond ◽  
Sarah C. Moody ◽  
Yingying Liu ◽  
Mete Civelek ◽  
Claudio J. Villanueva ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Mitochondrial Dynamics ◽  
Mouse Strains ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Metabolic Genes ◽  
And Function

Mitochondrial dynamics refers to the constant remodeling of mitochondrial populations by multiple cellular pathways that help maintain mitochondrial health and function. Disruptions in mitochondrial dynamics often lead to mitochondrial dysfunction, which is frequently associated with disease in rodents and humans. Consistent with this, obesity is associated with reduced mitochondrial function in white adipose tissue, partly via alterations in mitochondrial dynamics. Several proteins, including the E3 ubiquitin ligase membrane-associated RING-CH-type finger 5 (MARCH5), are known to regulate mitochondrial dynamics; however, the role of these proteins in adipocytes has been poorly studied. Here, we show that MARCH5 is regulated by peroxisome proliferator-activated receptor-γ (PPARγ) during adipogenesis and is correlated with fat mass across a panel of genetically diverse mouse strains, in ob/ob mice, and in humans. Furthermore, manipulation of MARCH5 expression in vitro and in vivo alters mitochondrial function, affects cellular metabolism, and leads to differential regulation of several metabolic genes. Thus our data demonstrate an association between mitochondrial dynamics and metabolism that defines MARCH5 as a critical link between these interconnected pathways.

scholarly journals Challenges and Opportunities for the Prevention and Treatment of Cardiovascular Disease Among Young Adults: Report From a National Heart, Lung, and Blood Institute Working Group

2020 ◽  
Vol 9 (19) ◽  
Author(s):  
Holly C. Gooding ◽  
Samuel S. Gidding ◽  
Andrew E. Moran ◽  
Nicole Redmond ◽  
Norrina B. Allen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Young Adults ◽  
Cardiovascular Health ◽  
Overweight And Obesity ◽  
Blood Institute ◽  
National Heart ◽  
Prevention And Treatment ◽  
Challenges And Opportunities ◽  
National Heart Lung

Abstract Improvements in cardiovascular disease (CVD) rates among young adults in the past 2 decades have been offset by increasing racial/ethnic and gender disparities, persistence of unhealthy lifestyle habits, overweight and obesity, and other CVD risk factors. To enhance the promotion of cardiovascular health among young adults 18 to 39 years old, the medical and broader public health community must understand the biological, interpersonal, and behavioral features of this life stage. Therefore, the National Heart, Lung, and Blood Institute, with support from the Office of Behavioral and Social Science Research, convened a 2‐day workshop in Bethesda, Maryland, in September 2017 to identify research challenges and opportunities related to the cardiovascular health of young adults. The current generation of young adults live in an environment undergoing substantial economic, social, and technological transformations, differentiating them from prior research cohorts of young adults. Although the accumulation of clinical and behavioral risk factors for CVD begins early in life, and research suggests early risk is an important determinant of future events, few trials have studied prevention and treatment of CVD in participants <40 years old. Building an evidence base for CVD prevention in this population will require the engagement of young adults, who are often disconnected from the healthcare system and may not prioritize long‐term health. These changes demand a repositioning of existing evidence‐based treatments to accommodate new sociotechnical contexts. In this article, the authors review the recent literature and current research opportunities to advance the cardiovascular health of today's young adults.

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