Mitochondrial Dysfunction in Atherosclerosis

Madamanchi, Nageswara R.; Runge, Marschall S.

doi:10.1161/01.res.0000258450.44413.96

Cited by 638 publications

(506 citation statements)

References 212 publications

(177 reference statements)

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“…It is important to note that although this study focused on the relationship between apoE4-induced ER stress and macrophage efferocytosis and apoptosis, mitochondrial dysfunction in macrophages has also been reported to promote inflammation (47). Additionally, mitochondrial dysfunction has also been associated with increased risk of atherosclerosis (48) and diabetes (49). Thus, it is possible that apoE4 expression may also induce mitochondrial abnormalities in macrophages and promote inflammation through this additional mechanism.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress

Cash

Kuhel

Basford

et al. 2012

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress

Cash

Kuhel

Basford

et al. 2012

Journal of Biological Chemistry

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“…Mitochondrial-derived oxidative stress has also been implicated in chronic inflammation, cancer progression (206), diabetes mellitus (148,152,(317)(318)(319)378), and atherosclerosis (21,258). Mitochondrial-derived ROS (MtROS) also contributes to LPS-mediated production of pro-inflammatory cytokines IL-1b, IL-6, and TNF-a (48).…”

Section: B Mitochondrial-derived Ros In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,266

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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“…Any factor that affects normal brain function (such as AD risk factors including TBI, ischemia, hypercholesterolemia, atherosclerosis) could facilitate perturbations in energy metabolism. For example, TBI is known to cause oxidative stress (Uryu et al, 2002), and mitochondrial dysfunction is induced by the major precursors of atherosclerosis (hypercholesterolemia, hyperglycemia) and is clearly associated with atherosclerosis or cardiomyopathy in humans and animal models of oxidative stress (reviewed in Madamanchi and Runge, 2007). Indeed, young adults carrying the ApoE4 allele, and MCI patients, exhibit reduced brain glucose metabolism (Reiman et al, 1996;Small et al, 2000;Mosconi et al, 2004;Mosconi, 2005), indicating that impaired energy metabolism may be an early contributing event to AD pathology rather than a consequence of the disease process.…”

Section: Cellular Changes Associated With Vascular Diseases Can Elevamentioning

confidence: 99%

Linking vascular disorders and Alzheimer's disease: Potential involvement of BACE1

Cole¹,

Vassar²

2009

Neurobiology of Aging

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The etiology of Alzheimer's disease (AD) remains unknown. However, specific risk factors have been identified, and aging is the strongest AD risk factor. The majority of cardiovascular events occur in older people and a close relationship between vascular disorders and AD exists. Amyloid plaques, composed of the beta amyloid peptide (Aβ), are hallmark lesions in AD and evidence indicates that Aβ plays a central role in AD pathophysiology. The BACE1 enzyme is essential for Aβ generation, and BACE1 levels are elevated in AD brain. The cause(s) of this BACE1 elevation remains undetermined. Here we review the potential contribution of vascular disease to AD pathogenesis. We examine the putative vasoactive properties of Aβ and how the cellular changes associated with vascular disease may elevate BACE1 levels. Despite increasing evidence, the exact role(s) vascular disorders play in AD remains to be determined. However, given that vascular diseases can be addressed by lifestyle and pharmacologic interventions, the potential benefits of these therapies in delaying the clinical appearance and progression of AD may warrant investigation.

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Mitochondrial Dysfunction in Atherosclerosis

Cited by 638 publications

References 212 publications

Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress

Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress

Reactive Oxygen Species in Inflammation and Tissue Injury

Linking vascular disorders and Alzheimer's disease: Potential involvement of BACE1

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