The mitochondrial permeability transition from in vitro artifact to disease target

By P. Bernardi, A. Krauskopf, E. Basso, V. Petronilli, Elizabeth Blalchy‐Dyson, F. Di Lisa, M. Forte. The FEBS Journal, 2006

638 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1dd7da651164e2aba6f4b92316bf0c3a362b1481

How researchers see this paper

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

In Molecular Biology

1. K. Yip
2. P. Pinton
3. C. Giorgi
4. R. Rizzuto
5. D. Bailey
6. E. Murphy
7. John Calvin Reed
8. Federico Fogolari

Citations in the corpus

• Bcl-2 family proteins and cancer (2008, background): “…mitochondrial membrane permeability transition, releasing apoptogenic proteins from mitochondria and stimulating reactive oxygen species production (Bernardi et al., 2006); (b) Ca2þ -sensitive mitochondrial fission protein Drp-1 (Szabadkai et al., 2004), which has been implicated in…”
• Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “The MPT opens under conditions of high Ca 2+ , ROS, high NADH, depletion of adenine nucleotides and loss of Δψ (103, 109, 110); conditions that occur during ischemia-reperfusion (24, 65).”
• Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death (2007, methodology): “On the basis of biochemical evidence, the standard model for the MPT pore consists of Vdac in the outer mitochondrial membrane, Ant in the inner mitochondrial membrane and cyclophilin D in the matri”
• Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “…highly debated, but the main players in mPTP assembly seem to include the adenine nucleotide transporter (ANT) in the inner membrane, the voltage-dependent anion channel (VDAC), the peripheral benzodiazepine receptor in the outer membrane and cyclophilin D, a matrix protein (Bernardi et al., 2006).”
• Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning (2007, background): “A key component of mitochondrial response to stress is the formation of the mPTP, a nonspecific, multimeric pore structure spanning the mitochondrial inner and outer membranes (Halestrap and Brenner, 2003; Bernardi et al., 2006).”
• Calcium and ROS: A mutual interplay (2015, background): “Mitochondrial permeability transition pore (mPTP) is a voltage and Ca2þ-dependent, cyclosporin A sensitive, high conductance channel, whose prolonged opening leads to a brisk increase in the permeability of the inner mitochondrial membrane to solutes with molecular mass up to 1500 Da [13].”
• 13 reasons why the brain is susceptible to oxidative stress (2018, background): “opens the mitochondrial permeability transition pore (mPTP) [54].”
• Dimers of mitochondrial ATP synthase form the permeability transition pore (2013, background): “Because a current is only seen with the dimers, it is logical to conclude that the PTP forms at the membrane interface two adjacent F O sectors, which would be in keeping with the well-characterized effects of fatty acids and lysophospholipids on the PTP (1).”