Role of oxidative stress in the process of vascular remodeling following coronary revascularization

Giovanna Gallo, Giorgia Pierelli, Maurizio Forte, Roberta Coluccia, Massimo Volpe, Speranza Rubattu

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Percutaneous coronary interventions (PCI), including balloon angioplasty and implantation of both bare metal and drug eluting coronary stents, are associated with risk of restenosis and in-stent thrombosis. A better understanding of signals that regulate cellular proliferation, neointimal formation and vessel wall thickening following PCI may contribute to identify novel preventive and therapeutic strategies aimed to reduce the atherosclerosis progression and the consequent vascular sequelae. Among the possible mechanisms, an increased level of reactive oxygen species (ROS) is associated with endothelial dysfunction and vascular smooth muscle cells (VSMCs) proliferation and migration involved in the post-procedural remodeling process. This review article provides an overview of the current knowledge on the contribution of increased oxidative stress to the post-procedural pathological vascular changes. We discuss the role of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide synthase, and of proteins regulating the mitochondrial function and dynamics. We will also highlight new knowledge on the atypical Fat1 cadherin that appears to play a key role in VSMCs proliferation. In fact, its induction after vascular injury serves as a physiological regulator of VSMCs growth. Specific molecular mechanisms, including Pin1- and H2S-mediated pathways, have been identified in the vascular complications of type 2 diabetic patients. The identification of novel key players may expand our perspectives and promote the development of new tools for future preventive and therapeutic strategies in order to reduce the adverse vascular remodeling following PCI. The latter represents one of the major goals in the development of innovative technologies with relevance for clinical practice.

Original languageEnglish
Pages (from-to)27-33
Number of pages7
JournalInternational Journal of Cardiology
Volume268
DOIs
Publication statusPublished - Oct 1 2018

Fingerprint

Percutaneous Coronary Intervention
Vascular Smooth Muscle
Smooth Muscle Myocytes
Oxidative Stress
Cell Proliferation
Blood Vessels
Mitochondrial Dynamics
Diabetic Angiopathies
Drug-Eluting Stents
Balloon Angioplasty
Vascular System Injuries
Cadherins
NADP
Nitric Oxide Synthase
Cell Movement
Stents
Reactive Oxygen Species
Atherosclerosis
Oxidoreductases
Thrombosis

Keywords

  • Coronary revascularization
  • In-stent thrombosis
  • Mitochondria
  • NADPH
  • Reactive oxygen species
  • Restenosis
  • Vascular smooth muscle cells

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Role of oxidative stress in the process of vascular remodeling following coronary revascularization",
abstract = "Percutaneous coronary interventions (PCI), including balloon angioplasty and implantation of both bare metal and drug eluting coronary stents, are associated with risk of restenosis and in-stent thrombosis. A better understanding of signals that regulate cellular proliferation, neointimal formation and vessel wall thickening following PCI may contribute to identify novel preventive and therapeutic strategies aimed to reduce the atherosclerosis progression and the consequent vascular sequelae. Among the possible mechanisms, an increased level of reactive oxygen species (ROS) is associated with endothelial dysfunction and vascular smooth muscle cells (VSMCs) proliferation and migration involved in the post-procedural remodeling process. This review article provides an overview of the current knowledge on the contribution of increased oxidative stress to the post-procedural pathological vascular changes. We discuss the role of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide synthase, and of proteins regulating the mitochondrial function and dynamics. We will also highlight new knowledge on the atypical Fat1 cadherin that appears to play a key role in VSMCs proliferation. In fact, its induction after vascular injury serves as a physiological regulator of VSMCs growth. Specific molecular mechanisms, including Pin1- and H2S-mediated pathways, have been identified in the vascular complications of type 2 diabetic patients. The identification of novel key players may expand our perspectives and promote the development of new tools for future preventive and therapeutic strategies in order to reduce the adverse vascular remodeling following PCI. The latter represents one of the major goals in the development of innovative technologies with relevance for clinical practice.",
keywords = "Coronary revascularization, In-stent thrombosis, Mitochondria, NADPH, Reactive oxygen species, Restenosis, Vascular smooth muscle cells",
author = "Giovanna Gallo and Giorgia Pierelli and Maurizio Forte and Roberta Coluccia and Massimo Volpe and Speranza Rubattu",
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T1 - Role of oxidative stress in the process of vascular remodeling following coronary revascularization

AU - Gallo, Giovanna

AU - Pierelli, Giorgia

AU - Forte, Maurizio

AU - Coluccia, Roberta

AU - Volpe, Massimo

AU - Rubattu, Speranza

PY - 2018/10/1

Y1 - 2018/10/1

N2 - Percutaneous coronary interventions (PCI), including balloon angioplasty and implantation of both bare metal and drug eluting coronary stents, are associated with risk of restenosis and in-stent thrombosis. A better understanding of signals that regulate cellular proliferation, neointimal formation and vessel wall thickening following PCI may contribute to identify novel preventive and therapeutic strategies aimed to reduce the atherosclerosis progression and the consequent vascular sequelae. Among the possible mechanisms, an increased level of reactive oxygen species (ROS) is associated with endothelial dysfunction and vascular smooth muscle cells (VSMCs) proliferation and migration involved in the post-procedural remodeling process. This review article provides an overview of the current knowledge on the contribution of increased oxidative stress to the post-procedural pathological vascular changes. We discuss the role of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide synthase, and of proteins regulating the mitochondrial function and dynamics. We will also highlight new knowledge on the atypical Fat1 cadherin that appears to play a key role in VSMCs proliferation. In fact, its induction after vascular injury serves as a physiological regulator of VSMCs growth. Specific molecular mechanisms, including Pin1- and H2S-mediated pathways, have been identified in the vascular complications of type 2 diabetic patients. The identification of novel key players may expand our perspectives and promote the development of new tools for future preventive and therapeutic strategies in order to reduce the adverse vascular remodeling following PCI. The latter represents one of the major goals in the development of innovative technologies with relevance for clinical practice.

AB - Percutaneous coronary interventions (PCI), including balloon angioplasty and implantation of both bare metal and drug eluting coronary stents, are associated with risk of restenosis and in-stent thrombosis. A better understanding of signals that regulate cellular proliferation, neointimal formation and vessel wall thickening following PCI may contribute to identify novel preventive and therapeutic strategies aimed to reduce the atherosclerosis progression and the consequent vascular sequelae. Among the possible mechanisms, an increased level of reactive oxygen species (ROS) is associated with endothelial dysfunction and vascular smooth muscle cells (VSMCs) proliferation and migration involved in the post-procedural remodeling process. This review article provides an overview of the current knowledge on the contribution of increased oxidative stress to the post-procedural pathological vascular changes. We discuss the role of nicotinamide adenine dinucleotide phosphate oxidase, nitric oxide synthase, and of proteins regulating the mitochondrial function and dynamics. We will also highlight new knowledge on the atypical Fat1 cadherin that appears to play a key role in VSMCs proliferation. In fact, its induction after vascular injury serves as a physiological regulator of VSMCs growth. Specific molecular mechanisms, including Pin1- and H2S-mediated pathways, have been identified in the vascular complications of type 2 diabetic patients. The identification of novel key players may expand our perspectives and promote the development of new tools for future preventive and therapeutic strategies in order to reduce the adverse vascular remodeling following PCI. The latter represents one of the major goals in the development of innovative technologies with relevance for clinical practice.

KW - Coronary revascularization

KW - In-stent thrombosis

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KW - Reactive oxygen species

KW - Restenosis

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