Role of the mitochondrial permeability transition in myocardial disease.

By J. Weiss, P. Korge, H. Honda, P. Ping. Circulation Research, 2003

613 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/440ed0effaa1f3b5b4d76a4b1c231353862d1ff0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. B. J. Gersh
2. G. Heusch

In Molecular Biology

1. Guido Kroemer
2. Peter Vandenabeele
3. T. Vanden Berghe
4. G. Heusch
5. Y. Tsujimoto
6. M. Schneider
7. S. Shimizu
8. Beth Levine

In Pathology and Forensic Medicine

1. B. J. Gersh
2. G. Heusch

Citations in the corpus

• Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “Anoxic and ischemic damage can thus result in the uncoupling of oxidative phosphorylation [107– 109].”
• Targeting an antioxidant to mitochondria decreases cardiac ischemia‐reperfusion injury (2005, neutral): “fatty acids from reaching the muscle (8).”
• Superoxide Flashes in Single Mitochondria (2008, neutral): “More importantly, a rebound increase in superoxide flash activity (1.9-fold increase over control) is observed shortly after reoxygenation following anoxia (Figure 6C), a critical period of increased cell vulnerability to oxidative damage ( Weiss et al., 2003 ).”
• Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death (2005, background): “Finally, we investigated the role of CypD in ischaemia/reperfusion (I/R) injury, in which disturbance of Ca 2p homeostasis and generation of reactive oxygen species have been implicate”
• NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart (2010, background): “Increased production of ROS in the failing heart leads to mitochondrial permeability transition (mPT) (16), which causes matrix swelling, outer membrane rupture, release of apoptotic signaling molecules, such as cytochrome c, from the intermembrane space, and irreversible injury to the mitochondria ”
• The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. (2016, background): “Opening of the mitochondrial permeability transition pore (MPTP) is of major importance for necrotic and apoptotic cardiomyocyte death.(48) – 51 Autophagy is the process of lysosomal protein degradation, particularly of mitochondrial proteins (mitophagy) and serves for recycling of proteins; its rol”