Mechanisms of Plaque Progression and Complications

Caterina, Raffaele De; Zampolli, Antonella; Turco, Serena Del; Libby, Peter

doi:10.1002/9780470988473.ch3

Cited by 2 publications

(2 citation statements)

References 151 publications

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“…Inflammatory aspects are also the secretion of matrix and the collagenolytic degradation of the matrix by enzymes, mostly deriving from macrophages. Inflammation is therefore at the basis of all pathogenetic aspects of atherosclerosis, from lesion inception (the adhesion and migration of monocytes), 41, 42 to their growth (accumulation of cells and matrix), 43 up to their clinical emergence (plaque fissuring) 44 …”

Section: The Inflammatory Theory Of Atherosclerosismentioning

confidence: 99%

Pharmacological modulation of vascular inflammation in atherothrombosis

Caterina¹,

Massaro²,

Scoditti³

et al. 2010

Annals of the New York Academy of Sciences

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Vascular inflammation, especially at the level of endothelial cells, has been shown to play a pivotal role in the inception, progression, and clinical complications of atherosclerosis. The common denominators for the activation of inflammatory genes appear to be a small subset of transcription factors--among which include nuclear factor-κB, activator protein-1 (AP-1), and GATA--that function as the central hub of vascular inflammation. Strategies directed to inhibit both the secondary mediators and the primary triggers (atherosclerosis risk factors) appear viable to inhibit atherosclerosis. However, attempts have now been made to address the central hub of vascular inflammation. "Old" drugs, such as dipyridamole, can also now be revisited for properties related to inhibition of vascular inflammation, probably by acting on the common hub of inflammation.

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Section: The Inflammatory Theory Of Atherosclerosismentioning

confidence: 99%

Pharmacological modulation of vascular inflammation in atherothrombosis

Caterina¹,

Massaro²,

Scoditti³

et al. 2010

Annals of the New York Academy of Sciences

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“…These results provided new insights into endothelial responses to mechanical forces useful to understand the mechanisms underlying atherogenesis in the vessels affected by disturbed blood flow. In this respect, in vitro studies have shown that the regions particularly prone to atherosclerosis are areas of ECs subjected to reverse flow and recirculation, and characterized by temporal and spatial gradients of shear stress compared to ECs grown in static conditions [De Caterina et al, ]. It appears crucial to understand the initial molecular events in atherogenesis to define ECs gene expression profiles in various sites of normal arteries.…”

Section: Biomechanical and Biochemical Stresses And Ecs Heterogeneitymentioning

confidence: 99%

Tumor Necrosis Factor Related Apoptosis Inducing Ligand (Trail) in Endothelial Response to Biomechanical and Biochemical Stresses in Arteries

D'Auria

Centurione

et al. 2015

J of Cellular Biochemistry

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Shear stress is determined by three physical components described in a famous triad: blood flow, blood viscosity and vessel geometry. Through the direct action on endothelium, shear stress is able to radically interfere with endothelial properties and the physiology of the vascular wall. Endothelial cells (ECs) have also to sustain biochemical stresses represented by chemokines, growth factors, cytokines, complement, hormones, nitric oxide (NO), oxygen and reactive oxygen species (ROS). Many growth factors, cytokines, chemokines, hormones, and chemical substances, like NO, act and regulate endothelium functions and homeostasis. Among these cytokines Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL) has been assigned a regulatory role in ECs physiology and physiopathology. Thus, the aim of this review is to provide a general overview of the endothelial response pathways after different types of biomechanical and biochemical stress in in vitro models and to analyze the crucial role of TRAIL under pathological conditions of the cardiocirculatory system like atherosclerosis, coronary artery disease, and diabetes.

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Mechanisms of Plaque Progression and Complications

Cited by 2 publications

References 151 publications

Pharmacological modulation of vascular inflammation in atherothrombosis

Pharmacological modulation of vascular inflammation in atherothrombosis

Tumor Necrosis Factor Related Apoptosis Inducing Ligand (Trail) in Endothelial Response to Biomechanical and Biochemical Stresses in Arteries

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