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Study Results from Weill Cornell Medical College Update Understanding of Ischemia (Novel cardiolipin therapeutic protects endothelial mitochondria...

July 9, 2014



Study Results from Weill Cornell Medical College Update Understanding of Ischemia (Novel cardiolipin therapeutic protects endothelial mitochondria during renal ischemia and mitigates microvascular rarefaction, inflammation, and fibrosis)

By a News Reporter-Staff News Editor at Biotech Week -- Researchers detail new data in Ischemia. According to news reporting originating from New York City, New York, by NewsRx correspondents, research stated, "Microvascular rarefaction, or loss of microvascular density, is increasingly implicated in the progression from acute ischemic kidney injury to chronic kidney disease. Microvascular dropout results in chronic tissue hypoxia, interstitial inflammation, and fibrosis."

Our news editors obtained a quote from the research from Weill Cornell Medical College, "There is currently no therapeutic intervention for microvascular rarefaction. We hypothesize that capillary dropout begins with ischemic damage to endothelial mitochondria due to cardiolipin peroxidation, resulting in loss of cristae and the failure to regenerate ATP upon reperfusion. SS-31 is a cell-permeable peptide that targets the inner mitochondrial membrane and binds selectively to cardiolipin. It was recently shown to inhibit cardiolipin peroxidation by cytochrome c peroxidase activity, and it has been shown to protect mitochondrial cristae in proximal tubular cells during ischemia, and accelerated ATP recovery upon reperfusion. We found mitochondrial swelling and loss of cristae membranes in endothelial and medullary tubular epithelial cells after 45-min ischemia in the rat. The loss of cristae membranes limited the ability of these cells to regenerate ATP upon reperfusion and led to loss of vascular integrity and to tubular cell swelling. SS-31 prevented mitochondria swelling and protected cristae membranes in both endothelial and epithelial cells. By minimizing endothelial and epithelial cell injury, SS-31 prevented 'no-reflow' after ischemia and significantly reduced the loss of peritubular capillaries and cortical arterioles, interstitial inflammation, and fibrosis at 4 wk after ischemia."

According to the news editors, the research concluded: "These results suggest that mitochondria protection represents an upstream target for pharmacological intervention in microvascular rarefaction and fibrosis."

For more information on this research see: Novel cardiolipin therapeutic protects endothelial mitochondria during renal ischemia and mitigates microvascular rarefaction, inflammation, and fibrosis. American Journal of Physiology-Renal Physiology, 2014;306(9):F970-F980. American Journal of Physiology-Renal Physiology can be contacted at: Amer Physiological Soc, 9650 Rockville Pike, Bethesda, MD 20814, USA (see also Ischemia).

The news editors report that additional information may be obtained by contacting S.Y. Liu, Weill Cornell Med College, Res Program Mitochondrial Therapeut, New York, NY 10021, United States. Additional authors for this research include Y. Soong, S.V. Seshan and H.H. Szeto.

Keywords for this news article include: Kidney, Haptens, Surgery, Therapy, Ischemia, Cytoplasm, Immunology, Nephrology, Organelles, Reperfusion, Cardiolipins, Inflammation, Mitochondria, New York City, United States, Medical Devices, Blood Transfusion, Cellular Structures, Intracellular Space, Transfusion Medicine, Subcellular Fractions, North and Central America

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2014, NewsRx LLC


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Source: Biotech Week


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