Immunosuppressive treatments in acute myocardial infarction and stroke

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Abstract

Atherosclerosis is an inflammatory disease that involves formation of atherosclerotic lesions characterized by deposition of lipids and cell debris in the arterial wall, fibrosis and recruitment of various cell types including smooth muscle, endothelial, immune and foam cells. Progressive enlargement of the atherosclerotic plaques together with development of necrosis, intraplaque hemorrhage and ulceration results into rupture of the plaques, with subsequent exposure to thrombotic material and occlusion of the artery. These phenomena culminate in myocardial infarction when they occur in the coronary arteries or stroke when cerebral arteries are affected. Several lines of evidence indicated that innate and adaptive immunity tightly regulate atherogenesis. In particular, activated T cells influence the stability of the atherosclerotic plaque and promote disease progression. Experiments performed on suitable animal models allowed to identify CD4 + lymphocytes as the major T cell subpopulation involved in atherogenesis. Furthermore, immunophenotypic and functional analyses demonstrated that human and murine plaques contain predominantly CD4 + T Helper (T H)1 cells producing proinflammatory cytokines. Taken together, these observations have fostered the evaluation in preclinical models of whether or not immunosuppressive drugs may represent an efficacious therapeutic strategy for atherosclerosis-associated diseases. This review focuses on the role of innate and adaptive immunity in atherogenesis and atherosclerosis progression, and discusses the potential immunosuppressive approaches for the treatment of patients affected by acute myocardial infarction and stroke, with particular emphasis on the use of tacrolimus and stem cell transplantation.

Original languageEnglish
Pages (from-to)59-67
Number of pages9
JournalCurrent Pharmaceutical Biotechnology
Volume13
Issue number1
DOIs
Publication statusPublished - Jan 2012

Fingerprint

Immunosuppressive Agents
Atherosclerosis
Stroke
Myocardial Infarction
Adaptive Immunity
Atherosclerotic Plaques
Innate Immunity
Therapeutics
T-Lymphocytes
Foam Cells
Th1 Cells
Cerebral Arteries
Stem Cell Transplantation
Tacrolimus
Smooth Muscle Myocytes
Disease Progression
Rupture
Coronary Vessels
Fibrosis
Necrosis

Keywords

  • Antibodies
  • Atherosclerosis
  • Immunosuppressive therapy
  • Inflammation
  • Myocardial infarction
  • Stroke
  • T cells

ASJC Scopus subject areas

  • Pharmaceutical Science
  • Biotechnology

Cite this

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abstract = "Atherosclerosis is an inflammatory disease that involves formation of atherosclerotic lesions characterized by deposition of lipids and cell debris in the arterial wall, fibrosis and recruitment of various cell types including smooth muscle, endothelial, immune and foam cells. Progressive enlargement of the atherosclerotic plaques together with development of necrosis, intraplaque hemorrhage and ulceration results into rupture of the plaques, with subsequent exposure to thrombotic material and occlusion of the artery. These phenomena culminate in myocardial infarction when they occur in the coronary arteries or stroke when cerebral arteries are affected. Several lines of evidence indicated that innate and adaptive immunity tightly regulate atherogenesis. In particular, activated T cells influence the stability of the atherosclerotic plaque and promote disease progression. Experiments performed on suitable animal models allowed to identify CD4 + lymphocytes as the major T cell subpopulation involved in atherogenesis. Furthermore, immunophenotypic and functional analyses demonstrated that human and murine plaques contain predominantly CD4 + T Helper (T H)1 cells producing proinflammatory cytokines. Taken together, these observations have fostered the evaluation in preclinical models of whether or not immunosuppressive drugs may represent an efficacious therapeutic strategy for atherosclerosis-associated diseases. This review focuses on the role of innate and adaptive immunity in atherogenesis and atherosclerosis progression, and discusses the potential immunosuppressive approaches for the treatment of patients affected by acute myocardial infarction and stroke, with particular emphasis on the use of tacrolimus and stem cell transplantation.",
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AB - Atherosclerosis is an inflammatory disease that involves formation of atherosclerotic lesions characterized by deposition of lipids and cell debris in the arterial wall, fibrosis and recruitment of various cell types including smooth muscle, endothelial, immune and foam cells. Progressive enlargement of the atherosclerotic plaques together with development of necrosis, intraplaque hemorrhage and ulceration results into rupture of the plaques, with subsequent exposure to thrombotic material and occlusion of the artery. These phenomena culminate in myocardial infarction when they occur in the coronary arteries or stroke when cerebral arteries are affected. Several lines of evidence indicated that innate and adaptive immunity tightly regulate atherogenesis. In particular, activated T cells influence the stability of the atherosclerotic plaque and promote disease progression. Experiments performed on suitable animal models allowed to identify CD4 + lymphocytes as the major T cell subpopulation involved in atherogenesis. Furthermore, immunophenotypic and functional analyses demonstrated that human and murine plaques contain predominantly CD4 + T Helper (T H)1 cells producing proinflammatory cytokines. Taken together, these observations have fostered the evaluation in preclinical models of whether or not immunosuppressive drugs may represent an efficacious therapeutic strategy for atherosclerosis-associated diseases. This review focuses on the role of innate and adaptive immunity in atherogenesis and atherosclerosis progression, and discusses the potential immunosuppressive approaches for the treatment of patients affected by acute myocardial infarction and stroke, with particular emphasis on the use of tacrolimus and stem cell transplantation.

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