Deregulation of Mitochondrial Function: A Potential Common Theme for Cardiovascular Disease Development

2008 ◽  
pp. 165-189 ◽  
Author(s):  
Scott W. Ballinger
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
Disease Development ◽  
Common Theme

scholarly journals When the Balance Tips: Dysregulation of Mitochondrial Dynamics as a Culprit in Disease

2021 ◽  
Vol 22 (9) ◽  
pp. 4617
Author(s):  
Styliana Kyriakoudi ◽  
Anthi Drousiotou ◽  
Petros P. Petrou
Keyword(s):  
Insulin Resistance ◽  
Mitochondrial Function ◽  
Human Disease ◽  
Molecular Mechanisms ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fusion ◽  
Mitochondrial Morphology ◽  
Disease Development ◽  
Pathological Conditions ◽  
Wide Range

Mitochondria are dynamic organelles, the morphology of which is tightly linked to their functions. The interplay between the coordinated events of fusion and fission that are collectively described as mitochondrial dynamics regulates mitochondrial morphology and adjusts mitochondrial function. Over the last few years, accruing evidence established a connection between dysregulated mitochondrial dynamics and disease development and progression. Defects in key components of the machinery mediating mitochondrial fusion and fission have been linked to a wide range of pathological conditions, such as insulin resistance and obesity, neurodegenerative diseases and cancer. Here, we provide an update on the molecular mechanisms promoting mitochondrial fusion and fission in mammals and discuss the emerging association of disturbed mitochondrial dynamics with human disease.

scholarly journals Mitochondrial Function, Biology, and Role in Disease

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
The United States ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Mitochondrial Defects ◽  
Exciting Time ◽  
Insight Into ◽  
Novel Therapeutic

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.

scholarly journals Intravenous Administration of Allogenic Cell-Derived Microvesicles of Healthy Origins Defends Against Atherosclerotic Cardiovascular Disease Development by a Direct Action on Endothelial Progenitor Cells

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 423 ◽  
Author(s):  
Nicoleta Alexandru ◽  
Eugen Andrei ◽  
Florentina Safciuc ◽  
Emanuel Dragan ◽  
Ana Maria Balahura ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Vascular Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Left Ventricular ◽  
Biologically Active ◽  
Atherosclerotic Cardiovascular Disease ◽  
Disease Development ◽  
Atherosclerotic Vascular Disease ◽  
Endothelial Progenitor

Atherosclerosis and cardiovascular disease development is the outcome of intermediate processes where endothelial dysfunction and vascular inflammation are main protagonists. Cell-derived microvesicles (MVs), endothelial progenitor cells (EPCs), and circulating microRNAs (miRNAs) are known as biomarkers and potential regulators for atherosclerotic vascular disease, but their role in the complexity of the inflammatory process and in the mechanism of vascular restoration is far from clear. We aimed to evaluate the biological activity and functional role of MVs, in particular of the EPCs-derived MVs (MVEs), of healthy origins in reducing atherosclerotic vascular disease development. The experiments were performed on hamsters divided into the following groups: simultaneously hypertensive–hyperlipidemic (HH group) by combining two feeding conditions for 4 months; HH with retro-orbital sinus injection containing 1 × 105 MVs or MVEs from control hamsters, one dose per month for 4 months of HH diet, to prevent atherosclerosis (HH-MVs or HH-MVEs group); and controls (C group), age-matched normal healthy animals. We found that circulating MV and MVE transplantation of healthy origins significantly reduces atherosclerosis development via (1) the mitigation of dyslipidemia, hypertension, and circulating EPC/cytokine/chemokine levels and (2) the structural and functional remodeling of arterial and left ventricular walls. We also demonstrated that (1) circulating MVs contain miRNAs; this was demonstrated by validating MVs and MVEs as transporters of Ago2-miRNA, Stau1-miRNA, and Stau2-miRNA complexes and (2) MV and MVE administration significantly protect against atherosclerotic cardiovascular disease via transfer of miR-223, miR-21, miR-126, and miR-146a to circulating late EPCs. It should be mentioned that the favorable effects of MVEs were greater than those of MVs. Our findings suggest that allogenic MV and MVE administration of healthy origins could counteract HH diet-induced detrimental effects by biologically active miR-10a, miR-21, miR-126, and miR-146a transfer to circulating EPCs, mediating their vascular repair function in atherosclerosis processes.

Prevalence of Metabolic Syndrome in Hemodialysis Patients Follow-Up for Three Years: Relationship with Cardiovascular Disease Development

2018 ◽  
Vol 04 (01) ◽  
Author(s):  
Ben Omrane Sioud Olfa ◽  
El Ati Zohra ◽  
Machfar Hanen ◽  
Knani Ines ◽  
Bouzidi Hassan ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Hemodialysis Patients ◽  
Disease Development

Adiponectin and cardiovascular disease: state of the art?

2007 ◽  
Vol 292 (4) ◽  
pp. H1655-H1663 ◽  
Author(s):  
Paul E. Szmitko ◽  
Hwee Teoh ◽  
Duncan J. Stewart ◽  
Subodh Verma
Keyword(s):  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Disease Risk ◽  
State Of The Art ◽  
Cardiovascular Disease Risk ◽  
Vascular Complications ◽  
Molecular Pathways ◽  
Disease Development ◽  
Active Participant ◽  
Current Review

The cardiometabolic syndrome, associated with increased cardiovascular disease risk in the industrialized world, is estimated to affect one in four adults. Although the mechanisms linking obesity and cardiovascular disease remain unclear, research continues to unravel the molecular pathways behind this pandemic. Adipose tissue has emerged as a metabolically active participant in mediating vascular complications, serving as an active endocrine and paracrine organ secreting adipokines, which participate in diverse metabolic processes. Among these adipokines is adiponectin, which seems to possess antiatherogenic and anti-inflammatory effects and may be protective against cardiovascular disease development. The current review describes the pathophysiology of adiponectin in atherosclerotic disease.

scholarly journals Potassium and magnesium deficiency, its role in cardiovascular disease development and possibilities of correction

2019 ◽  
Vol 21 (1) ◽  
pp. 67-73
Author(s):  
Galina A. Baryshnikova ◽  
◽  
Svetlana A. Chorbinskaya ◽  
Irina I. Stepanova ◽  
Olga E. Blokhina ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Magnesium Deficiency ◽  
Disease Development

scholarly journals Structure of Lipoproteins and Their Capacity for Lipid Exchange: Relevance for Development of Atherosclerosis and Its Treatment by HDL Therapy

2021 ◽  
Author(s):  
Sarah Waldie ◽  
Rita Del Giudice ◽  
Marité Cárdenas
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoproteins ◽  
Western World ◽  
Disease Development ◽  
Lipid Transfer ◽  
Artery Wall ◽  
Unsaturated Lipids ◽  
Clinical Observations ◽  
Lipid Exchange ◽  
The Difference

Atherosclerosis, the largest killer in the western world, arises from build-up of plaques at the artery walls and can result in cardiovascular disease. Low- and high-density lipoproteins are involved in the disease development by depositing and removing lipids to and from macrophages at the artery wall. These processes are complex and not fully understood. Thus, determining the specific roles of the different lipoprotein fractions involved is of fundamental importance for the treatment of the disease. In this chapter, we present the state of the art in lipoprotein structure with focus on the comparison between normolipidemic and hypertriglyceridemic individuals. Then we discuss lipid transfer between lipoproteins and receptor-free cellular membranes. Although these models lack any receptor, key clinical observations are mirrored by these, including increased ability of HDL to remove lipids, in contrast to the ability of LDL to deposit them. Also effects of saturated and unsaturated lipids in the presence and absence of cholesterol are revised. These models can then be used to understand the difference in functionality of lipoproteins from individuals showing different lipid profiles and have the potential to be used also for the development of new HDL therapies.

Early life stress in mice alters gut microbiota independent of maternal microbiota inheritance

2021 ◽  
Vol 320 (5) ◽  
pp. R663-R674
Author(s):  
Keri M. Kemp ◽  
Jackson Colson ◽  
Robin G. Lorenz ◽  
Craig L. Maynard ◽  
Jennifer S. Pollock
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Disease ◽  
Gut Microbiota ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Microbial Community Composition ◽  
Early Life Stress ◽  
Alpha Diversity ◽  
Disease Development

Exposure to early life stress (ELS) is associated with a greater risk of chronic disease development including depression and cardiovascular disease. Altered gut microbiota has been linked to both depression and cardiovascular disease in mice and humans. Rodent models of early life neglect are used to characterize the mechanistic links between early life stress (ELS) and the risk of disease later in life. However, little is understood about ELS exposure and the gut microbiota in the young mice and the influence of the maternal inheritance of the gut microbiota. We used a mouse model of ELS, maternal separation with early weaning (MSEW), and normally reared mice to determine whether the neonate microbiota is altered, and if so, are the differences attributable to changes in dam microbiota that are then transmitted to their offspring. Individual amplicon sequence variants (ASVs) displayed differential abundance in the microbiota of MSEW compared with normally reared pups at postnatal day ( PD) 28. Additionally, ELS exposure reduced the alpha diversity and altered microbial community composition at PD28. The composition, levels of alpha diversity, and abundance of individual ASVs in the microbiota of dams were similar from MSEW or normally reared cohorts. Thus, the observed shifts in the abundance of individual bacterial ASVs in the neonates and young pups are likely driven by endogenous effects of MSEW in the offspring host and are not due to inherited differences from the dam. This knowledge suggests that exposure to ELS has a direct effect on microbial factors on the risk of chronic disease development.

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