Myocardial ischemia and metabolic disorder

Takashi Yokota, Shintaro Kinugawa, Hiroyuki Tsutsui

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

During myocardial ischemia, the heart acutely adapts to the restricted supply of oxygen and substrates, and undergoes a dramatic switch from aerobic to anaerobic metabolism. However, this alteration in energy metabolism may cause calcium overload, the onset of mitochondrial permeability transition, and the activation of apoptotic cascades as well as reduced ATP synthesis in the myocardium, which contributes to a functional damage to the myocardium. Moreover, cardiac mitochondria are major sources of reactive oxygen species during ischemia, which may cause myocardial injury and contribute to poor recovery of myocardial dysfunction after reperfusion. Therefore, the modulation of mitochondrial function could be key therapeutics for cardiac protection during ischemia and reperfusion.

Original languageEnglish
Pages (from-to)621-624
Number of pages4
JournalNippon rinsho. Japanese journal of clinical medicine
Volume68
Issue number4
Publication statusPublished - Jan 1 2010
Externally publishedYes

Fingerprint

Reperfusion
Myocardial Ischemia
Myocardium
Ischemia
Anaerobiosis
Energy Metabolism
Permeability
Reactive Oxygen Species
Mitochondria
Adenosine Triphosphate
Oxygen
Calcium
Wounds and Injuries
Therapeutics

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Myocardial ischemia and metabolic disorder. / Yokota, Takashi; Kinugawa, Shintaro; Tsutsui, Hiroyuki.

In: Nippon rinsho. Japanese journal of clinical medicine, Vol. 68, No. 4, 01.01.2010, p. 621-624.

Research output: Contribution to journalReview article

Yokota, Takashi ; Kinugawa, Shintaro ; Tsutsui, Hiroyuki. / Myocardial ischemia and metabolic disorder. In: Nippon rinsho. Japanese journal of clinical medicine. 2010 ; Vol. 68, No. 4. pp. 621-624.
@article{a97e96bf27d24a8f85334c0f09b45423,
title = "Myocardial ischemia and metabolic disorder",
abstract = "During myocardial ischemia, the heart acutely adapts to the restricted supply of oxygen and substrates, and undergoes a dramatic switch from aerobic to anaerobic metabolism. However, this alteration in energy metabolism may cause calcium overload, the onset of mitochondrial permeability transition, and the activation of apoptotic cascades as well as reduced ATP synthesis in the myocardium, which contributes to a functional damage to the myocardium. Moreover, cardiac mitochondria are major sources of reactive oxygen species during ischemia, which may cause myocardial injury and contribute to poor recovery of myocardial dysfunction after reperfusion. Therefore, the modulation of mitochondrial function could be key therapeutics for cardiac protection during ischemia and reperfusion.",
author = "Takashi Yokota and Shintaro Kinugawa and Hiroyuki Tsutsui",
year = "2010",
month = "1",
day = "1",
language = "English",
volume = "68",
pages = "621--624",
journal = "Astrophysical Journal",
issn = "0004-637X",
publisher = "IOP Publishing Ltd.",
number = "4",

}

TY - JOUR

T1 - Myocardial ischemia and metabolic disorder

AU - Yokota, Takashi

AU - Kinugawa, Shintaro

AU - Tsutsui, Hiroyuki

PY - 2010/1/1

Y1 - 2010/1/1

N2 - During myocardial ischemia, the heart acutely adapts to the restricted supply of oxygen and substrates, and undergoes a dramatic switch from aerobic to anaerobic metabolism. However, this alteration in energy metabolism may cause calcium overload, the onset of mitochondrial permeability transition, and the activation of apoptotic cascades as well as reduced ATP synthesis in the myocardium, which contributes to a functional damage to the myocardium. Moreover, cardiac mitochondria are major sources of reactive oxygen species during ischemia, which may cause myocardial injury and contribute to poor recovery of myocardial dysfunction after reperfusion. Therefore, the modulation of mitochondrial function could be key therapeutics for cardiac protection during ischemia and reperfusion.

AB - During myocardial ischemia, the heart acutely adapts to the restricted supply of oxygen and substrates, and undergoes a dramatic switch from aerobic to anaerobic metabolism. However, this alteration in energy metabolism may cause calcium overload, the onset of mitochondrial permeability transition, and the activation of apoptotic cascades as well as reduced ATP synthesis in the myocardium, which contributes to a functional damage to the myocardium. Moreover, cardiac mitochondria are major sources of reactive oxygen species during ischemia, which may cause myocardial injury and contribute to poor recovery of myocardial dysfunction after reperfusion. Therefore, the modulation of mitochondrial function could be key therapeutics for cardiac protection during ischemia and reperfusion.

UR - http://www.scopus.com/inward/record.url?scp=77951652168&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77951652168&partnerID=8YFLogxK

M3 - Review article

C2 - 20387551

AN - SCOPUS:77951652168

VL - 68

SP - 621

EP - 624

JO - Astrophysical Journal

JF - Astrophysical Journal

SN - 0004-637X

IS - 4

ER -