Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium

Goro Asano, En Takashi, Toshiyuki Ishiwata, Munehiko Onda, Munehiro Yokoyama, Zenya Naito, Muhammad Ashraf, Yuhichi Sugisaki

Research output: Contribution to journalReview article

48 Citations (Scopus)

Abstract

The important factors that influence the progress of ischemic cardiac lesion are blood flow condition and abnormal cardiac metabolism. Myocardial ischemia is promoted by either an increase in oxygen demand or a shortage of oxygen supply. The Na+-Ca++ ATPase ion exchange mechanism is very important for myocardial contraction and cell damage. Na+ - K+ATPase and Ca++ ATPase are enzyme histochemically localized in subsarcolemmal cisterns, sarcolemmal reticulum and capillary endothelium, and keep myocardial function. These ATPases are impaired by anoxia, superoxides and free radicals. The reduction of O2 results in the production of superoxides as well as hydrogen peroxide (H2O 2). H2O2 is highly diffusible and induces cell damage. H2O2 appears to affect not only lipids but also intramembranous proteins embedded in the cell membrane. The hydroxyl radical (OH) also participates in lipid hyperoxidation. In the pathogenesis of ischemic and/or reperfused heart disease, ischemia induces rapid or gradual changes in all membrane systems and causes reversible or irreversible injury including necrotic and apoptotic cell death. Advanced glycation end products (AGEs) accumulation induced by diabetic conditioning is an etiologic factor inducing cardiomyopathy. The AGEs protein affects cell changes such as increased number, transformation, functional disturbance and cytokine elimination. In coronary arteries, the migration of smooth muscle cells caused by the taking up of AGEs proteins through the receptor (RAGE), and cytokine discharge are suggested. AGEs accumulation may induce diabetic macroangiopathy through RAGE, and the increase in the level of RAGE expression by endothelial cells could be a reason that diabetes mellitus accelerates atherosclerosis. On the other hand, we also reported that hyperglycemia was a promoting factor of ischemic heart injury in diabetic animals. Ischemic preconditioning is a useful phenomenon that limits myocardial damage. We foused on protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and mitochondrial ATP-dependent potassium (mitoK ATP) channel as mediator or end which effector are necessary for adaptation. The opening of the mitoKATP channel induces the depolarization of mitochondria, reducing Ca++overload during reperfusion. The regeneration of myocardial cells is confirmed using embryonic stem cells. Myocardial cells that exhibit self-pulsation are generated from mesenchymal stem cells in mesodermal tissues of the bone marrow.

Original languageEnglish (US)
Pages (from-to)384-392
Number of pages9
JournalJournal of Nippon Medical School
Volume70
Issue number5
DOIs
StatePublished - Oct 1 2003
Externally publishedYes

Fingerprint

Reperfusion Injury
Myocardium
Superoxides
Adenosine Triphosphatases
Heart Injuries
Oxygen
Myocardial Contraction
Lipids
Ischemic Preconditioning
Reticulum
Advanced Glycosylation End Products
Proteins
Cytokine Receptors
Ion Exchange
Vascular Endothelium
Embryonic Stem Cells
Mitogen-Activated Protein Kinases
Mesenchymal Stromal Cells
Cardiomyopathies
Hyperglycemia

Keywords

  • AGEs preconditioning
  • ATPase depletion
  • Hydrogen peroxide
  • Ischemic cardiomyopathy

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Asano, G., Takashi, E., Ishiwata, T., Onda, M., Yokoyama, M., Naito, Z., ... Sugisaki, Y. (2003). Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium. Journal of Nippon Medical School, 70(5), 384-392. https://doi.org/10.1272/jnms.70.384

Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium. / Asano, Goro; Takashi, En; Ishiwata, Toshiyuki; Onda, Munehiko; Yokoyama, Munehiro; Naito, Zenya; Ashraf, Muhammad; Sugisaki, Yuhichi.

In: Journal of Nippon Medical School, Vol. 70, No. 5, 01.10.2003, p. 384-392.

Research output: Contribution to journalReview article

Asano, G, Takashi, E, Ishiwata, T, Onda, M, Yokoyama, M, Naito, Z, Ashraf, M & Sugisaki, Y 2003, 'Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium', Journal of Nippon Medical School, vol. 70, no. 5, pp. 384-392. https://doi.org/10.1272/jnms.70.384
Asano G, Takashi E, Ishiwata T, Onda M, Yokoyama M, Naito Z et al. Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium. Journal of Nippon Medical School. 2003 Oct 1;70(5):384-392. https://doi.org/10.1272/jnms.70.384
Asano, Goro ; Takashi, En ; Ishiwata, Toshiyuki ; Onda, Munehiko ; Yokoyama, Munehiro ; Naito, Zenya ; Ashraf, Muhammad ; Sugisaki, Yuhichi. / Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium. In: Journal of Nippon Medical School. 2003 ; Vol. 70, No. 5. pp. 384-392.
@article{244243233f3a465ab8087cd52a3250d7,
title = "Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium",
abstract = "The important factors that influence the progress of ischemic cardiac lesion are blood flow condition and abnormal cardiac metabolism. Myocardial ischemia is promoted by either an increase in oxygen demand or a shortage of oxygen supply. The Na+-Ca++ ATPase ion exchange mechanism is very important for myocardial contraction and cell damage. Na+ - K+ATPase and Ca++ ATPase are enzyme histochemically localized in subsarcolemmal cisterns, sarcolemmal reticulum and capillary endothelium, and keep myocardial function. These ATPases are impaired by anoxia, superoxides and free radicals. The reduction of O2 results in the production of superoxides as well as hydrogen peroxide (H2O 2). H2O2 is highly diffusible and induces cell damage. H2O2 appears to affect not only lipids but also intramembranous proteins embedded in the cell membrane. The hydroxyl radical (OH) also participates in lipid hyperoxidation. In the pathogenesis of ischemic and/or reperfused heart disease, ischemia induces rapid or gradual changes in all membrane systems and causes reversible or irreversible injury including necrotic and apoptotic cell death. Advanced glycation end products (AGEs) accumulation induced by diabetic conditioning is an etiologic factor inducing cardiomyopathy. The AGEs protein affects cell changes such as increased number, transformation, functional disturbance and cytokine elimination. In coronary arteries, the migration of smooth muscle cells caused by the taking up of AGEs proteins through the receptor (RAGE), and cytokine discharge are suggested. AGEs accumulation may induce diabetic macroangiopathy through RAGE, and the increase in the level of RAGE expression by endothelial cells could be a reason that diabetes mellitus accelerates atherosclerosis. On the other hand, we also reported that hyperglycemia was a promoting factor of ischemic heart injury in diabetic animals. Ischemic preconditioning is a useful phenomenon that limits myocardial damage. We foused on protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and mitochondrial ATP-dependent potassium (mitoK ATP) channel as mediator or end which effector are necessary for adaptation. The opening of the mitoKATP channel induces the depolarization of mitochondria, reducing Ca++overload during reperfusion. The regeneration of myocardial cells is confirmed using embryonic stem cells. Myocardial cells that exhibit self-pulsation are generated from mesenchymal stem cells in mesodermal tissues of the bone marrow.",
keywords = "AGEs preconditioning, ATPase depletion, Hydrogen peroxide, Ischemic cardiomyopathy",
author = "Goro Asano and En Takashi and Toshiyuki Ishiwata and Munehiko Onda and Munehiro Yokoyama and Zenya Naito and Muhammad Ashraf and Yuhichi Sugisaki",
year = "2003",
month = "10",
day = "1",
doi = "10.1272/jnms.70.384",
language = "English (US)",
volume = "70",
pages = "384--392",
journal = "Journal of Nippon Medical School",
issn = "1345-4676",
publisher = "Medical Association of Nippon Medical School",
number = "5",

}

TY - JOUR

T1 - Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium

AU - Asano, Goro

AU - Takashi, En

AU - Ishiwata, Toshiyuki

AU - Onda, Munehiko

AU - Yokoyama, Munehiro

AU - Naito, Zenya

AU - Ashraf, Muhammad

AU - Sugisaki, Yuhichi

PY - 2003/10/1

Y1 - 2003/10/1

N2 - The important factors that influence the progress of ischemic cardiac lesion are blood flow condition and abnormal cardiac metabolism. Myocardial ischemia is promoted by either an increase in oxygen demand or a shortage of oxygen supply. The Na+-Ca++ ATPase ion exchange mechanism is very important for myocardial contraction and cell damage. Na+ - K+ATPase and Ca++ ATPase are enzyme histochemically localized in subsarcolemmal cisterns, sarcolemmal reticulum and capillary endothelium, and keep myocardial function. These ATPases are impaired by anoxia, superoxides and free radicals. The reduction of O2 results in the production of superoxides as well as hydrogen peroxide (H2O 2). H2O2 is highly diffusible and induces cell damage. H2O2 appears to affect not only lipids but also intramembranous proteins embedded in the cell membrane. The hydroxyl radical (OH) also participates in lipid hyperoxidation. In the pathogenesis of ischemic and/or reperfused heart disease, ischemia induces rapid or gradual changes in all membrane systems and causes reversible or irreversible injury including necrotic and apoptotic cell death. Advanced glycation end products (AGEs) accumulation induced by diabetic conditioning is an etiologic factor inducing cardiomyopathy. The AGEs protein affects cell changes such as increased number, transformation, functional disturbance and cytokine elimination. In coronary arteries, the migration of smooth muscle cells caused by the taking up of AGEs proteins through the receptor (RAGE), and cytokine discharge are suggested. AGEs accumulation may induce diabetic macroangiopathy through RAGE, and the increase in the level of RAGE expression by endothelial cells could be a reason that diabetes mellitus accelerates atherosclerosis. On the other hand, we also reported that hyperglycemia was a promoting factor of ischemic heart injury in diabetic animals. Ischemic preconditioning is a useful phenomenon that limits myocardial damage. We foused on protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and mitochondrial ATP-dependent potassium (mitoK ATP) channel as mediator or end which effector are necessary for adaptation. The opening of the mitoKATP channel induces the depolarization of mitochondria, reducing Ca++overload during reperfusion. The regeneration of myocardial cells is confirmed using embryonic stem cells. Myocardial cells that exhibit self-pulsation are generated from mesenchymal stem cells in mesodermal tissues of the bone marrow.

AB - The important factors that influence the progress of ischemic cardiac lesion are blood flow condition and abnormal cardiac metabolism. Myocardial ischemia is promoted by either an increase in oxygen demand or a shortage of oxygen supply. The Na+-Ca++ ATPase ion exchange mechanism is very important for myocardial contraction and cell damage. Na+ - K+ATPase and Ca++ ATPase are enzyme histochemically localized in subsarcolemmal cisterns, sarcolemmal reticulum and capillary endothelium, and keep myocardial function. These ATPases are impaired by anoxia, superoxides and free radicals. The reduction of O2 results in the production of superoxides as well as hydrogen peroxide (H2O 2). H2O2 is highly diffusible and induces cell damage. H2O2 appears to affect not only lipids but also intramembranous proteins embedded in the cell membrane. The hydroxyl radical (OH) also participates in lipid hyperoxidation. In the pathogenesis of ischemic and/or reperfused heart disease, ischemia induces rapid or gradual changes in all membrane systems and causes reversible or irreversible injury including necrotic and apoptotic cell death. Advanced glycation end products (AGEs) accumulation induced by diabetic conditioning is an etiologic factor inducing cardiomyopathy. The AGEs protein affects cell changes such as increased number, transformation, functional disturbance and cytokine elimination. In coronary arteries, the migration of smooth muscle cells caused by the taking up of AGEs proteins through the receptor (RAGE), and cytokine discharge are suggested. AGEs accumulation may induce diabetic macroangiopathy through RAGE, and the increase in the level of RAGE expression by endothelial cells could be a reason that diabetes mellitus accelerates atherosclerosis. On the other hand, we also reported that hyperglycemia was a promoting factor of ischemic heart injury in diabetic animals. Ischemic preconditioning is a useful phenomenon that limits myocardial damage. We foused on protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and mitochondrial ATP-dependent potassium (mitoK ATP) channel as mediator or end which effector are necessary for adaptation. The opening of the mitoKATP channel induces the depolarization of mitochondria, reducing Ca++overload during reperfusion. The regeneration of myocardial cells is confirmed using embryonic stem cells. Myocardial cells that exhibit self-pulsation are generated from mesenchymal stem cells in mesodermal tissues of the bone marrow.

KW - AGEs preconditioning

KW - ATPase depletion

KW - Hydrogen peroxide

KW - Ischemic cardiomyopathy

UR - http://www.scopus.com/inward/record.url?scp=0242558032&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0242558032&partnerID=8YFLogxK

U2 - 10.1272/jnms.70.384

DO - 10.1272/jnms.70.384

M3 - Review article

C2 - 14578938

AN - SCOPUS:0242558032

VL - 70

SP - 384

EP - 392

JO - Journal of Nippon Medical School

JF - Journal of Nippon Medical School

SN - 1345-4676

IS - 5

ER -