Programmed death as a therapeutic target to reduce myocardial infarction

Keith A Webster

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

In the United States, angioplasty or bypass surgery to remove coronary occlusions is performed on approximately two million patients each year. Although reperfusion is essential for salvaging ischemic myocardium, it also promotes infarction by activating programmed cell death in the formerly ischemic tissue. Reperfusion injury begins when oxidative stress and calcium accumulation by the mitochondria cause activation of the so-called mitochondrial death channels. These channels have become the focus of evolving strategies to protect the heart from infarction. Preclinical and preliminary clinical studies indicate that agents with diverse modes of action can reduce infarct size by 50% or more and significantly preserve myocardial functions. This article reviews the most advanced pharmacological approaches for their ability to reduce infarct size by inhibiting the mitochondrial death pathways.

Original languageEnglish
Pages (from-to)492-499
Number of pages8
JournalTrends in Pharmacological Sciences
Volume28
Issue number9
DOIs
StatePublished - Sep 1 2007

Fingerprint

Salvaging
Mitochondria
Oxidative stress
Cell death
Surgery
Infarction
Chemical activation
Myocardial Infarction
Tissue
Mitochondrial Size
Calcium
Coronary Occlusion
Reperfusion Injury
Angioplasty
Reperfusion
Myocardium
Oxidative Stress
Cell Death
Pharmacology
Therapeutics

ASJC Scopus subject areas

  • Pharmacology
  • Toxicology

Cite this

Programmed death as a therapeutic target to reduce myocardial infarction. / Webster, Keith A.

In: Trends in Pharmacological Sciences, Vol. 28, No. 9, 01.09.2007, p. 492-499.

Research output: Contribution to journalArticle

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