doi: 10.1161/CIRCRESAHA.107.170225
© 2008 American Heart Association, Inc.
Editorials |
Toll-Like Receptor Signaling
Defensive or Offensive for the Heart?
From the Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Japan.
Correspondence to Prof Masatsugu Hori, Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail mhori@medone.med.osaka-u.ac.jp
See related article, pages 257–264
Key Words: Toll-like receptor 4 • innate immune • remodeling • myocardial infarction
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The majority of cardiovascular diseases cause progressive deterioration, mainly resulting from accumulation of vascular and myocardial tissue damage. A growing body of evidence indicates that oxidative stress and the inflammatory response are involved as triggers or mediators of these tissue injuries.1 It is well known that atherosclerosis is an inflammatory disease preferentially occurring in lesion-prone areas. Bacterial infections such as Chlamydia pneumoniae and cytomegalovirus could cause the inflammatory response of the coronary arteries, and accumulation of macrophages in the vascular wall promotes plaque formation. In myocardial infarction, infiltration of macrophages and neutrophils may modify myocardial injury even after reperfusion. It is also reported that inflammatory cytokines and growth factors are activated in either ischemic or nonischemic chronic heart failure. In such progressively deteriorating conditions, both oxidative stress and the inflammatory response are synergistically involved, causing a vicious cycle of progression of injury. These considerations support the hypothesis that inflammatory response is involved in most progressive cardiovascular diseases.
The innate immune system is the first line of defensive mechanisms that protect hosts from invading microbial pathogens. The Toll-like receptor (TLR) family plays a fundamental role in the innate immune response.2,3 In 1997, vertebrate homologs of the Drosophila spp transmembrane pattern recognition receptor "Toll" were identified and termed TLRs. Among the 11 human TLRs identified to date, TLR1, -2, -4, -5, and -6 are all present on the plasma membrane. TLR1, -2, -4, and -6 recognize lipids, whereas TLR5 recognizes protein ligands. Among those, TLR4 recognizes specific components of Gram-negative bacteria lipopolysaccharide
Related Article:
Circ. Res. 2008 102: 257-264.