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Mitochondria are highly dynamic organelles beyond powerhouses of a cell. These components also play important roles in cell homeostasis by regulating cell function and phenotypic modulation. Atherosclerosis is the leading cause of morbidity and mortality in developed and developing countries. Mitochondrial dysfunction has been increasingly associated with the initiation and progression of atherosclerosis by elevating the production of reactive oxygen species and mitochondrial oxidative stress damage, mitochondrial dynamics dysfunction, and energy supply. In this review, we describe the progression of the link between mitochondrial dysfunction and atherosclerosis and its potential regulation mechanisms.
This article was published in the following journal.
Name: DNA and cell biology
Sepsis is associated with disturbed glucose metabolism and reduced mitochondrial activity and biogenesis, ultimately leading to multiple organ dysfunction, e.g., acute kidney injury (AKI). Cystathioni...
Erectile dysfunction (ED) is frecuent in HIV infected patients and it can be associated with atherosclerosis and cardiovascular events. So, the objetive was to evaluate whether the presence of moderat...
Chronic intermittent hypoxia (CIH) induces systemic (hypertension) and central (mitochondrial dysfunction underlying cognitive deficits). We hypothesized that agonists of oestradiol receptors (ER) α ...
Alzheimer's disease (AD) patients display widespread mitochondrial defects. Brain hypometabolism occurs alongside mitochondrial defects, and correlates well with cognitive decline. Numerous theories a...
Mitochondrial dysfunction is a causative and/or exacerbating feature of many pathologies. We discuss below approaches to modulate mitochondrial dysfunction that involve (1) increasing their energetic ...
Aim #1 To investigate the prevalence, risk and correlation of the level of sepsis with mitochondrial dysfunction in sepsis patients Aim 1.1 To investigate the prevalence of mitochondria dy...
An association between insulin resistance and mitochondrial dysfunction has been observed in aging, T2D, and in offspring of patients with T2D. It remains to be determined whether pharmac...
The primary aim of the study is to demonstrate that mitochondrial dysfunction occurs in both skeletal muscle and circulating platelets of severely septic and septic shock ICU-admitted pati...
Mitochondrial diseases occur due to inadequate energy production. In addition, nitric oxide (NO) deficiency occurs in mitochondrial diseases. The endothelial layer of blood vessels functio...
This study will be a Phase 2, randomized, double-blind, placebo-controlled study, enrolling 45 elderly subjects with previous evidence of mitochondrial dysfunction to evaluate whether the ...
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.
A heterogenous group of disorders characterized by alterations of mitochondrial metabolism that result in muscle and nervous system dysfunction. These are often multisystemic and vary considerably in age at onset (usually in the first or second decade of life), distribution of affected muscles, severity, and course. (From Adams et al., Principles of Neurology, 6th ed, pp984-5)
In vitro fertilization technique that uses mitochondrial DNA from a healthy donor in order to prevent the transmission of MITOCHONDRIAL DISEASE.
Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.
Mitochondrial anion carrier proteins that function as dimers and form proton channels in the INNER MITOCHONDRIAL MEMBRANE which creates proton leaks and uncouples OXIDATIVE PHOSPHORYLATION from ATP synthesis, resulting in the generation of heat instead of ATP.