title: Tumor Necrosis Factor Related Apoptosis Inducing Ligand (Trail) in endothelial response to biomechanical and biochemical stresses in arteries.
abstract: 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.
authors.affiliation: Department of Cardiac and Vascular Surgery, Campus Bio-Medico University of Rome, Rome, Italy.
authors.forename: F
authors.initials: F
authors.lastname: D'Auria
authors.affiliation: Department of Medicine and Ageing Sciences, G. d'Annunzio University, Chieti, Pescara, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Centurione
authors.affiliation: Institute of Molecular Genetics, National Research Council-Pavia, Section of Chieti, Italy.
authors.forename: M A
authors.initials: MA
authors.lastname: Centurione
authors.affiliation: Department of Medicine and Ageing Sciences, G. d'Annunzio University, Chieti, Pescara, Italy.|Ageing Research Center, CeSI, G. d'Annunzio University Foundation, Chieti, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Angelini
authors.affiliation: Department of Medicine and Ageing Sciences, G. d'Annunzio University, Chieti, Pescara, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Di Pietro
mesh_terms: D000818:Animals; D001158:Arteries / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D050197:Atherosclerosis / Q000378:metabolism / Q000503:physiopathology; D001696:Biomechanical Phenomena; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000378:metabolism / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D066298:In Vitro Techniques; D013312:Stress, Physiological; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism*
chemical_list: D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human
keywords: CARDIOVASCULAR SYSTEM; ENDOTHELIAL CELLS; SHEAR STRESS; TRAIL; VASCULAR SMOOTH MUSCLE CELLS