Cell Death and Diabetic Cardiomyopathy

Lu Cai, Yujian Kang

Research output: Contribution to journalReview article

117 Citations (Scopus)

Abstract

Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and animal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of the mechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death process. Several studies have shown that suppression of myocardial cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy.

Original languageEnglish (US)
Pages (from-to)219-228
Number of pages10
JournalCardiovascular Toxicology
Volume3
Issue number3
DOIs
StatePublished - Oct 31 2003
Externally publishedYes

Fingerprint

Diabetic Cardiomyopathies
Cell death
Cell Death
Medical problems
Reactive Nitrogen Species
Poisons
Cardiomyopathies
Reperfusion
Reactive Oxygen Species
Atherosclerosis
Animals
Chronic Disease
Ischemia
Animal Models
Antioxidants
Myocardial Infarction
Apoptosis

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Toxicology

Cite this

Cell Death and Diabetic Cardiomyopathy. / Cai, Lu; Kang, Yujian.

In: Cardiovascular Toxicology, Vol. 3, No. 3, 31.10.2003, p. 219-228.

Research output: Contribution to journalReview article

Cai, Lu ; Kang, Yujian. / Cell Death and Diabetic Cardiomyopathy. In: Cardiovascular Toxicology. 2003 ; Vol. 3, No. 3. pp. 219-228.
@article{773a745ac7274b60a02eab4b19c00948,
title = "Cell Death and Diabetic Cardiomyopathy",
abstract = "Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and animal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of the mechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death process. Several studies have shown that suppression of myocardial cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy.",
author = "Lu Cai and Yujian Kang",
year = "2003",
month = "10",
day = "31",
doi = "10.1385/CT:3:3:219",
language = "English (US)",
volume = "3",
pages = "219--228",
journal = "Cardiovascular Toxicology",
issn = "1530-7905",
publisher = "Humana Press",
number = "3",

}

TY - JOUR

T1 - Cell Death and Diabetic Cardiomyopathy

AU - Cai, Lu

AU - Kang, Yujian

PY - 2003/10/31

Y1 - 2003/10/31

N2 - Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and animal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of the mechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death process. Several studies have shown that suppression of myocardial cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy.

AB - Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and animal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of the mechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death process. Several studies have shown that suppression of myocardial cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy.

UR - http://www.scopus.com/inward/record.url?scp=0142117335&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0142117335&partnerID=8YFLogxK

U2 - 10.1385/CT:3:3:219

DO - 10.1385/CT:3:3:219

M3 - Review article

VL - 3

SP - 219

EP - 228

JO - Cardiovascular Toxicology

JF - Cardiovascular Toxicology

SN - 1530-7905

IS - 3

ER -