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 language | English |
|---|---|
| Pages (from-to) | 384-391 |
| Number of pages | 8 |
| Journal | American Scientist |
| Volume | 97 |
| Issue number | 5 |
| DOIs | |
| State | Published - Sep 1 2009 |
Fingerprint
ASJC Scopus subject areas
- General
Cite this
Research output: Contribution to journal › Article
}
TY - JOUR
T1 - 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
AU - Webster, Keith A
PY - 2009/9/1
Y1 - 2009/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=69949102241&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=69949102241&partnerID=8YFLogxK
U2 - 10.1511/2009.80.384
DO - 10.1511/2009.80.384
M3 - Article
VL - 97
SP - 384
EP - 391
JO - American Scientist
JF - American Scientist
SN - 0003-0996
IS - 5
ER -