Mitochondria and Cell Death, 1st Edition by David M. Hockenbery (eds.)

By David M. Hockenbery (eds.)

This quantity examines the position of mitochondria in numerous varieties of mobile loss of life, together with apoptotic and necrotic cellphone deaths. subject matters mentioned comprise mitochondrial outer membrane permeabilization (MOMP) and the permeability transition pore; center procedures similar to calcium dealing with, fission and fusion, reactive oxygen species iteration, and upkeep of mitochondrial DNA constancy and protein folding homeostasis; and retrograde signaling among mitochondria and different mobile parts, together with the $64000 position of mitochondria in antiviral immunity. The expertly authored chapters are drawn from multidisciplinary overseas views, lending a nuanced and complete method of the fabric. Mitochondria and mobilephone Death, a part of the Cell dying in Biology and Diseases sequence, is priceless interpreting for graduate scholars, researchers, and clinicians within the fields of neuroscience, oncology, gastroenterology, and hepatology, in addition to these drawn to the learn of mitochondria and mobile biology.

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ROS and high [Ca2+]m). 2 Possible Mechanism(s) Behind IP Protection To date, it is still not clear how IP affects [Ca2+]i dynamics during ischemia or during the reperfusion that follows. These critical questions remain open primarily due to the lack of quantitative reports where the measurements of Ca2+ are of high enough spatiotemporal resolution to permit measurement of [Ca2+]i signaling events such as Ca2+ sparks and [Ca2+]i transients. The available information about [Ca2+]i and IP is derived from NMR measurements or fluorescence measurements of [Ca2+]i from whole hearts.

559633 Chen Y-R, Zweier JL (2014) Cardiac mitochondria and reactive oxygen species generation. Circ Res 114:524–537. 300559 2 Mitochondrial Calcium and Ischemia: Reperfusion Injury in Heart 37 Chen EP, Bittner HB, Davis RD, Folz RJ, Van Trigt P (1996) Extracellular superoxide dismutase transgene overexpression preserves postischemic myocardial function in isolated murine hearts. Circulation 94:II412–II417 Chen Z, Siu B, Ho YS, Vincent R, Chua CC, Hamdy RC, Chua BH (1998) Overexpression of MnSOD protects against myocardial ischemia/reperfusion injury in transgenic mice.

Circ J 77:1111–1122 Fieni F, Lee SB, Jan YN, Kirichok Y (2012) Activity of the mitochondrial calcium uniporter varies greatly between tissues. Nat Commun 3:1317. 1038/ncomms2325 Fieni F, Johnson DE, Hudmon A, Kirichok Y (2014) Mitochondrial Ca2+ uniporter and CaMKII in heart. Nature 513:E1–E2. 1038/nature13626 Franzini-Armstrong C (2007) ER-mitochondria communication. How privileged? Physiology (Bethesda) 22:261–268. 2007 Fuller W, Parmar V, Eaton P, Bell JR, Shattock MJ (2003) Cardiac ischemia causes inhibition of the Na/K ATPase by a labile cytosolic compound whose production is linked to oxidant stress.

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