Cells, cytokines and cellular immunity in the pathogenesis of fibroproliferative vasculopathies

Research output: Contribution to journalReview article

19 Citations (Scopus)

Abstract

Atherosclerosis and restenosis are the result of vascular injury followed by an inflammatory and fibroproliferative response that involves a large number of growth factors, cytokines, and cellular elements. Platelet activation and leukocyte recruitment into the arterial intima play a crucial role, initiating a whole spectrum of reactions leading to vascular smooth muscle cell hyperplasia and intimal migration. The roles of macrophages and lymphocytes and mast cells as mediators of inflammation and immune response is discussed, as are the roles of growth factors and cytokines. New light on the Old' problems will help us to devise newer and better therapeutic strategies to combat these clinical entities.

Original languageEnglish
Pages (from-to)701-715
Number of pages15
JournalCanadian Journal of Physiology and Pharmacology
Volume83
Issue number8-9
DOIs
StatePublished - Aug 2005

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Tunica Intima
Cellular Immunity
Intercellular Signaling Peptides and Proteins
Cytokines
Inflammation Mediators
Vascular System Injuries
Platelet Activation
Vascular Smooth Muscle
Mast Cells
Smooth Muscle Myocytes
Hyperplasia
Atherosclerosis
Leukocytes
Macrophages
Lymphocytes
Light
Therapeutics

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology

Cite this

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AB - Atherosclerosis and restenosis are the result of vascular injury followed by an inflammatory and fibroproliferative response that involves a large number of growth factors, cytokines, and cellular elements. Platelet activation and leukocyte recruitment into the arterial intima play a crucial role, initiating a whole spectrum of reactions leading to vascular smooth muscle cell hyperplasia and intimal migration. The roles of macrophages and lymphocytes and mast cells as mediators of inflammation and immune response is discussed, as are the roles of growth factors and cytokines. New light on the Old' problems will help us to devise newer and better therapeutic strategies to combat these clinical entities.

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