Mitochondrial death channels in heart attacks, cells die if they aren't -perfused with fresh oxygen-and kill themselves if they are. Understanding cell suicide may greatly improve outcomes

Keith A Webster

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Mitochondrial death channels play a big role in causing coronary artery diseases among humans, which calls for understanding cell suicide to prevent this phenomenon. The mitochondrion, which provides power to cells, is the main player in defining the outcome of heart attacks. Mitochondria have cellular poisons that are normally sequestered in inactive form, but can trigger cell suicide when activated. These suicide regulators are discharged from mitochondria through mitochondrial death channels. The mitochondrial electron-transport chain is a series of protein-metal complexes entrenched in the mitochondrial inner membrane that have increased reduction potentials. The mitochondrial death channels incorporate the mitochondrial permeability transition pore (mPTP) and the mitochondrial apoptosis channel. The mAC causes apoptosis by creating a channel in the outer mitochondrial membrane that facilitates the discharge of cytochrome c, a mobile electron carrier in the electron-transport chain. Cytochrome c reacts with other proteins in the cell cytoplasm to create an apoptosome.

Original languageEnglish
Pages (from-to)384-391
Number of pages8
JournalAmerican Scientist
Volume97
Issue number5
DOIs
StatePublished - Sep 1 2009

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Suicide
Myocardial Infarction
Oxygen
Mitochondria
Mitochondrial Membranes
Electron Transport
Cytochromes c
Apoptosomes
Apoptosis
Poisons
Coordination Complexes
Coronary Artery Disease
Cytoplasm
Proteins
Electrons

ASJC Scopus subject areas

  • General

Cite this

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