Associations between atherosclerosis and neurological diseases, beyond ischemia-induced cerebral damage

Colín-Castelán, Dannia; Zaina, Silvio

doi:10.1007/s11154-019-09486-z

Cited by 14 publications

(10 citation statements)

References 137 publications

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“…Prevalence of atherosclerosis increases with population ageing. Among the dangerous and life-threatening consequences of atherosclerosis are ischemic heart disease and stroke that can develop when the disease affects the arteries feeding the heart and the brain correspondingly [1]. Atherosclerosis is a chronic disease, which can remain asymptomatic during a long period of time.…”

Section: Introductionmentioning

confidence: 99%

“…Pathogenesis of atherosclerosis includes many known factors, such as alterations of lipid metabolism, oxidative stress, changes in the immune system functioning, and decreased tissue response to injury. Accumulating evidence reveals that atherosclerosis shares some pathophysiological mechanisms with other chronic human diseases, including cancers and neurological disorders [1,4,5].…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Salnikova

Orekhova

Grechko

et al. 2021

IJMS

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Altered mitochondrial function is currently recognized as an important factor in atherosclerosis initiation and progression. Mitochondrial dysfunction can be caused by mitochondrial DNA (mtDNA) mutations, which can be inherited or spontaneously acquired in various organs and tissues, having more or less profound effects depending on the tissue energy status. Arterial wall cells are among the most vulnerable to mitochondrial dysfunction due to their barrier and metabolic functions. In atherosclerosis, mitochondria cause alteration of cellular metabolism and respiration and are known to produce excessive amounts of reactive oxygen species (ROS) resulting in oxidative stress. These processes are involved in vascular disease and chronic inflammation associated with atherosclerosis. Currently, the list of known mtDNA mutations associated with human pathologies is growing, and many of the identified mtDNA variants are being tested as disease markers. Alleviation of oxidative stress and inflammation appears to be promising for atherosclerosis treatment. In this review, we discuss the role of mitochondrial dysfunction in atherosclerosis development, focusing on the key cell types of the arterial wall involved in the pathological processes. Accumulation of mtDNA mutations in isolated arterial wall cells, such as endothelial cells, may contribute to the development of local inflammatory process that helps explaining the focal distribution of atherosclerotic plaques on the arterial wall surface. We also discuss antioxidant and anti-inflammatory approaches that can potentially reduce the impact of mitochondrial dysfunction.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Salnikova

Orekhova

Grechko

et al. 2021

IJMS

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“…In the present study, we indicate several novel findings: (1) HCD-fed model rats showed declined acquisition of a learning and memory paradigm in the MWM, indicating that cognitive dysfunctions in rats could be induced by chronic cerebral hypoperfusion as well as hypercholesterolemia; (2) we identified that ICAM-1, VCAM-1, and E-selectin in cerebral microvessels of HCD-fed model rats were upregulated, suggesting that the combination of sustained hypoperfusion and hypercholesterolemia promoted cerebral microvascular endothelial activation; and (3) carotid atherosclerosis and concomitant dietary hypercholesterolemia induced alterations in the expression of NPY in hypothalamus, the level of plasma leptin and proinflammatory markers such as TNF-α, IL-1β, and CRP in the circulation, as well as TNF-α and IL-1β in the cerebral cortex. These changes suggest perturbations in the bidirectional communication between neuronal, endocrine, and immune systems correlated with cerebral ischemia-associated comorbidity factors such as carotid atherosclerosis and hypercholesterolemia that might be related to high risk for future cerebrovascular events ( Colín-Castelán and Zaina, 2019 ); interventions with curcumin helped to beneficially attenuate carotid lumen stenosis, modulate lipid metabolism, improve learning and memory impairments, ameliorate inflammation reactions in the cerebral microvasculature, and regulate neuroendocrine-immune changes in this complex rat model of experimental ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

“…Carotid artery atherosclerosis, as one of the major causes of cerebrovascular disease, has been implicated in the etiology of stroke, cognitive impairment, and dementia ( Muller et al, 2007 ; Carrington Rice et al, 2009 ; Romero et al, 2009 ). Epidemiological evidence exists to support the idea that neurological dysfunction and carotid artery atherosclerosis will coexist for several years until the first evident neurological symptoms appear ( Colín-Castelán and Zaina, 2019 ). Growing data have demonstrated that hemodynamic changes in the cerebral circulation may be one of the important mechanisms underlying the association between carotid atherosclerosis and brain damage ( Muller et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

A Comorbid Rat Model of Neuroendocrine-Immune System Alterations Under the Impact of Risk Factors for Stroke

Wang

et al. 2022

Front. Aging Neurosci.

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Hypercholesterolemia and carotid atherosclerosis contribute to the etiology of stroke. However, there has been a lack of appropriate comorbid animal models incorporating some of the ubiquitous characteristics that precede strokes. Curcumin is a natural active polyphenolic compound extracted from the rhizoma of Curcuma longa L. which possesses comprehensive bioactivities. The present study aimed to evaluate whether neurobehavioral deficits, neuroendocrine-immune dysregulations and cerebral microcirculation dysfunction, are part of the initial stages of cerebral ischemia in individuals suffering from carotid atherosclerosis resulting from a high cholesterol diet (HCD) and if they could be tested using a comorbid animal model. Furthermore, the utility of this model will be examined following the administration of curcumin. Adult wild-type SD rats were fed a regular diet or HCD and supplemented with either vehicle or curcumin for 4 weeks. Carotid injury was induced by an air-drying endothelial denudation method at the end of the second week. Plasma cholesterol, carotid pathomorphology, neurobehavioral tests, and neuroendocrine-immune parameters were measured. We found higher plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), intima and media (I/M) ratio, but lower high-density lipoprotein-cholesterol (HDL-C), spatial learning and memory capacity impairment, elevated NPY expression in the hypothalamus, increased plasma concentration of leptin, upregulated TNF-α, IL-1β, and CRP in the circulation as well as TNF-α and IL-1β in the cerebral cortex, plus enhanced ICAM-1, VCAM-1, and E-selectin in cerebral microvessels in HCD-fed model rats. All these alterations were ameliorated by curcumin. These results suggest that a comorbid rat model was effectively developed by HCD and carotid injury.

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“…The formation of atherosclerotic plaques narrows the arterial lumen to increase the risk of myocardial infarction and stroke (2). When the plaques are formed in cerebral vessels, the cerebral atherosclerosis also contributes to development of cognitive impairment (3).…”

Section: Introductionmentioning

confidence: 99%

Fine-tuning of microglia polarization prevents diabetes-associated cerebral atherosclerosis

et al. 2022

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Diabetes increases the occurrence and severity of atherosclerosis. When plaques form in brain vessels, cerebral atherosclerosis causes thickness, rigidity, and unstableness of cerebral artery walls, leading to severe complications like stroke and contributing to cognitive impairment. So far, the molecular mechanism underlying cerebral atherosclerosis is not determined. Moreover, effective intervention strategies are lacking. In this study, we showed that polarization of microglia, the resident macrophage in the central nervous system, appeared to play a critical role in the pathological progression of cerebral atherosclerosis. Microglia likely underwent an M2c-like polarization in an environment long exposed to high glucose. Experimental suppression of microglia M2c polarization was achieved through transduction of microglia with an adeno-associated virus (serotype AAV-PHP.B) carrying siRNA for interleukin-10 (IL-10) under the control of a microglia-specific TMEM119 promoter, which significantly attenuated diabetes-associated cerebral atherosclerosis in a mouse model. Thus, our study suggests a novel translational strategy to prevent diabetes-associated cerebral atherosclerosis through in vivo control of microglia polarization.

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Associations between atherosclerosis and neurological diseases, beyond ischemia-induced cerebral damage

Cited by 14 publications

References 137 publications

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis

A Comorbid Rat Model of Neuroendocrine-Immune System Alterations Under the Impact of Risk Factors for Stroke

Fine-tuning of microglia polarization prevents diabetes-associated cerebral atherosclerosis

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