TY - JOUR
T1 - Spontaneous Myocardial Infarction and Nitric Oxide Synthase
AU - Tsutsui, Masato
AU - Nakata, Sei
AU - Shimokawa, Hiroaki
AU - Otsuji, Yutaka
AU - Yanagihara, Nobuyuki
N1 - Funding Information:
The authors' work presented in this article was supported in part by the Grants-in-Aid for Scientific Research (20390074, 16209027, 16659192, 17390071, 14570096) and the Grants-in-Aid for Exploratory Research (16650097, 16659209) from the Ministry of Education, Culture, Sports, Science and Technology, Tokyo, Japan, and the Japanese Ministry of Health, Labor, and Welfare (Tokyo, Japan), and by grants from the Yamanouchi Foundation for Research on Metabolic Disorders, the Research Foundation for Treatment of Metabolic Abnormalities (Osaka, Japan), the Sankyo Pharmaceutical Co (Tokyo, Japan), the Japan Heart Foundation Grant for Research on Arteriosclerosis Update (Tokyo, Japan), the Smoking Research Foundation (Tokyo, Japan), and the University of Occupational and Environmental Health for Advanced Research (Kitakyushu, Japan).
PY - 2008/11
Y1 - 2008/11
N2 - Myocardial infarction (MI) is caused by coronary atherosclerosis and/or arteriosclerosis. Because endothelial nitric oxide synthase (eNOS) exerts powerful antiatherosclerotic/antiarteriosclerotic effects, it is speculated that blockade of eNOS activity might result in MI. However, neither genetic disruption of eNOS nor pharmacologic inhibition of eNOS activity induces MI in animals. On the other hand, intriguingly, genetic disruption of all three nitric oxide synthase (NOS) isoforms (neuronal NOS, inducible NOS, and eNOS) spontaneously caused MI accompanied by multiple cardiovascular risk factors of metabolic origin in mice. This is the first in vivo demonstration showing that the defective NOS system is involved in the pathogenesis of spontaneous MI. Based on the evidence, this review summarizes our current knowledge of spontaneous MI and NOS.
AB - Myocardial infarction (MI) is caused by coronary atherosclerosis and/or arteriosclerosis. Because endothelial nitric oxide synthase (eNOS) exerts powerful antiatherosclerotic/antiarteriosclerotic effects, it is speculated that blockade of eNOS activity might result in MI. However, neither genetic disruption of eNOS nor pharmacologic inhibition of eNOS activity induces MI in animals. On the other hand, intriguingly, genetic disruption of all three nitric oxide synthase (NOS) isoforms (neuronal NOS, inducible NOS, and eNOS) spontaneously caused MI accompanied by multiple cardiovascular risk factors of metabolic origin in mice. This is the first in vivo demonstration showing that the defective NOS system is involved in the pathogenesis of spontaneous MI. Based on the evidence, this review summarizes our current knowledge of spontaneous MI and NOS.
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U2 - 10.1016/j.tcm.2008.12.002
DO - 10.1016/j.tcm.2008.12.002
M3 - Review article
C2 - 19345314
AN - SCOPUS:63249126340
SN - 1050-1738
VL - 18
SP - 275
EP - 279
JO - Trends in Cardiovascular Medicine
JF - Trends in Cardiovascular Medicine
IS - 8
ER -