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| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 2011;4(1):74-80
Review Article
Chemokines and Inflammation in Heart disease: Adaptive or Maladaptive?
Sima T. Tarzami
Departments of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York 10029, USA.
Received January 10, 2011; accepted February 3, 2011; Epub February 6, 2011; published February 28, 2011
Abstract: Heart disease is not only the leading cause of death, disability, and healthcare expense in the US, but also the leading cause
of death worldwide. Therefore, treatments to lessen ischemia-related cardiac damage could affect a broad swath of the population and
have significant health and fiscal impacts. Cardiac dysfunction has been associated with elevated circulating chemokine levels, both in
animals and humans. Most studies in this area have focused on chemokine expression as a prominent feature of the post-infarction
inflammatory response. Such studies have investigated the role of chemokines in inflammatory leukocyte recruitment. Other work on
this topic has focused on stem-cell therapy or factors e.g. chemokines mobilizing bone marrow progenitor cells as possible avenues
for improving contractile dysfunction. Findings from numerous preclinical studies and several initial clinical trials support the feasibility
of promoting the recruitment of bone marrow-derived cells to the infarcted heart and increased homing following injury, supporting the
notion that cell therapy might have therapeutic potential. They have not, however, addressed the possibility of an autocrine/paracrine
effect wherein the chemokine receptors, present on the cardiac myocyte surface, modulate functional responses to stress in which can
be adaptive or maladaptive in nature. (IJCEM1101003).
Keywords: Chemokines, stem-cell therapy, inflammation, myocardial infarction, congestive heart failure
Full Text PDF
Address all correspondence to:
Sima T. Tarzami, PhD
Mount Sinai School of Medicine, Department of Medicine
1 Gustave L Levy Place, Box 1030
New York, NY 10029, USA.
Tel: 212-241-8228, FAX: 212-241-4080.
E-mail: sima.tarzami@mssm.edu
Review Article
Chemokines and Inflammation in Heart disease: Adaptive or Maladaptive?
Sima T. Tarzami
Departments of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York 10029, USA.
Received January 10, 2011; accepted February 3, 2011; Epub February 6, 2011; published February 28, 2011
Abstract: Heart disease is not only the leading cause of death, disability, and healthcare expense in the US, but also the leading cause
of death worldwide. Therefore, treatments to lessen ischemia-related cardiac damage could affect a broad swath of the population and
have significant health and fiscal impacts. Cardiac dysfunction has been associated with elevated circulating chemokine levels, both in
animals and humans. Most studies in this area have focused on chemokine expression as a prominent feature of the post-infarction
inflammatory response. Such studies have investigated the role of chemokines in inflammatory leukocyte recruitment. Other work on
this topic has focused on stem-cell therapy or factors e.g. chemokines mobilizing bone marrow progenitor cells as possible avenues
for improving contractile dysfunction. Findings from numerous preclinical studies and several initial clinical trials support the feasibility
of promoting the recruitment of bone marrow-derived cells to the infarcted heart and increased homing following injury, supporting the
notion that cell therapy might have therapeutic potential. They have not, however, addressed the possibility of an autocrine/paracrine
effect wherein the chemokine receptors, present on the cardiac myocyte surface, modulate functional responses to stress in which can
be adaptive or maladaptive in nature. (IJCEM1101003).
Keywords: Chemokines, stem-cell therapy, inflammation, myocardial infarction, congestive heart failure
Full Text PDF
Address all correspondence to:
Sima T. Tarzami, PhD
Mount Sinai School of Medicine, Department of Medicine
1 Gustave L Levy Place, Box 1030
New York, NY 10029, USA.
Tel: 212-241-8228, FAX: 212-241-4080.
E-mail: sima.tarzami@mssm.edu
