Mitochondrial permeability transition: a common pathway to necrosis and apoptosis.

By Jae‐Sung Kim, Lihua He, J. Lemasters. Biochemical and Biophysical Research Communications - BBRC, 2003

783 citations recorded by the source corpus.

How researchers see this paper

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

AIF deficiency compromises oxidative phosphorylation (2004, background): “Fructose, known to readily fuel anaerobic glycolysis, but not galactose or sucrose, which poorly enter glycolysis ( Kim et al, 2003; Mazzio and Soliman, 2003), relieved the glucose dependence of AIF � /y cells.”
Mitochondrial Calcium and the Permeability Transition in Cell Death (2009, background): “In the MPT, large conductance permeability transition (PT) pores open that make the mitochondrial inner membrane abruptly permeable to all solutes of molecular weight up to about 1500 Da [2,21,25].”
Selective Mitochondrial Autophagy, or Mitophagy, as a Targeted Defense Against Oxidative Stress, Mitochondrial Dysfunction, and Aging (2005, positive): “9 However, with less severe stress, MPT pore formation appears to promote autophagy.”
Reactive Oxygen Species in Inflammation and Tissue Injury (2014, neutral): “The opening of the mPTP causes mitochondrial swelling due to massive influx of solute and water, resulting in mitochondrial depolarization and cessation of ATP synthesis (215).”
Pathophysiology of Acute Kidney Injury (2012, positive): “Substantial evidence suggests that the permeability is due to the opening of a nonspecific pore with a high conductance of molecules less than Mw ~ 1200 (105, 267).”