Intracellular calcium overloading and oxidative stress in cardiomyocyte necrosis via a mitochondriocentric signal-transducer-effector pathway

Mazen Shaheen, Yaser Cheema, Atta U. Shahbaz, Syamal Bhattacharya, Karl Weber

Research output: Contribution to journalReview article

5 Citations (Scopus)

Abstract

Congestive heart failure (CHF), a common clinical syndrome, has reached epidemic proportions. Its disabling symptoms account for frequent hospitalizations and readmissions. Pathophysiological mechanisms that lead to CHF and account for its progressive nature are of considerable interest. Important scientific observations obtained from Dr Pawan K Singal's laboratory in Winnipeg, Manitoba, have provided crucial insights to our understanding of the pathophysiological factors that contribute to cardiomyocyte necrosis (the heart is a postmitotic organ incapable of tolerating an ongoing loss of these cells without adverse functional consequences). This increment in knowledge and the mechanistic insights afforded by Dr Singal and his colleagues have highlighted the role of excessive intracellular calcium accumulation and the appearance of oxidative stress in CHF, in which the rate of reactive oxygen species generation overwhelms their rate of detoxification by antioxidant defenses. They have shown that this common pathophysiological scenario applies to diverse entities such as ischemia/reperfusion and hypoxia/reoxygenation forms of injury, myocardial infarction and the cardiomyopathies that accompany diabetes and excess levels of catecholamines and adriamycin. The authors are honoured to be invited to contribute to the present focus issue of Experimental & Clinical Cardiology in recognizing Dr Singal's numerous scholarly accomplishments. The present article reviews the authors' recent work on a mitochondriocentric signal-transducer-effector pathway to cardiomyocyte necrosis found in rats with either an acute stressor state that accompanies isoproterenol administration or a chronic stressor state manifested after four weeks of aldosterone/salt treatment.

Original languageEnglish (US)
Pages (from-to)109-115
Number of pages7
JournalExperimental and Clinical Cardiology
Volume16
Issue number4
StatePublished - Dec 2011

Fingerprint

Transducers
Cardiac Myocytes
Oxidative Stress
Necrosis
Heart Failure
Calcium
Manitoba
Cardiology
Aldosterone
Cardiomyopathies
Isoproterenol
Doxorubicin
Reperfusion
Catecholamines
Reactive Oxygen Species
Hospitalization
Ischemia
Salts
Antioxidants
Myocardial Infarction

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)
  • Physiology

Cite this

Intracellular calcium overloading and oxidative stress in cardiomyocyte necrosis via a mitochondriocentric signal-transducer-effector pathway. / Shaheen, Mazen; Cheema, Yaser; Shahbaz, Atta U.; Bhattacharya, Syamal; Weber, Karl.

In: Experimental and Clinical Cardiology, Vol. 16, No. 4, 12.2011, p. 109-115.

Research output: Contribution to journalReview article

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