Spontaneous Myocardial Infarction and Nitric Oxide Synthase

Masato Tsutsui, Sei Nakata, Hiroaki Shimokawa, Yutaka Otsuji, Nobuyuki Yanagihara

Research output: Contribution to journalReview articlepeer-review

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)275-279
Number of pages5
JournalTrends in Cardiovascular Medicine
Volume18
Issue number8
DOIs
Publication statusPublished - 2008 Nov

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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