By David M. Hockenbery (eds.)
This quantity examines the position of mitochondria in several kinds of mobile demise, together with apoptotic and necrotic mobilephone deaths. issues mentioned contain mitochondrial outer membrane permeabilization (MOMP) and the permeability transition pore; middle methods corresponding to calcium dealing with, fission and fusion, reactive oxygen species new release, and upkeep of mitochondrial DNA constancy and protein folding homeostasis; and retrograde signaling among mitochondria and different mobile elements, together with the $64000 position of mitochondria in antiviral immunity. The expertly authored chapters are drawn from multidisciplinary foreign views, lending a nuanced and entire method of the cloth. Mitochondria and phone Death, a part of the Cell demise in Biology and Diseases sequence, is important studying 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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Example text
The Ca2+ efflux in heart muscle cells is primarily mediated by the mitochondrial Na+/Ca2+ exchanger (NCLX), whose identity has only recently been identified (Palty et al. 2010). , net transfer of electrical charge), the dependency of NCLX on cytosolic Na+ ([Na+]i), and the magnitude of NCLX Ca2+ efflux [for further information on these topics see Boyman et al. (2013)]. Ischemia-induced changes in [Ca2+]m. It is a prevailing view that [Ca2+]m rises substantially during IR in heart; however, the mechanisms that may underlie such a rise remain unclear.
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. Cardiovasc Res 57:1044–1051 Fuller W, Eaton P, Bell JR, Shattock MJ (2004) Ischemia-induced phosphorylation of phospholemman directly activates rat cardiac Na/K-ATPase. FASEB J 18:197–199. 03-0213fje Gabel SA, Cross HR, London RE, Steenbergen C, Murphy E (1997) Decreased intracellular pH is not due to increased H+ extrusion in preconditioned rat hearts.
MPTP and [Ca2+]m. The vulnerability of the mitochondria to high Ca2+ was first reported over 60 years ago. The quantities of Ca2+ that were used in these studies were not sufficiently large to cause osmotic shock. It was therefore suggested that the observed mitochondrial swelling and dysfunction were due to a Ca2+-sensitive process (Raaflaub 1953; Hunter and Ford 1955; Nicholls and Akerman 1982). In 1986, Ibrahim Al-Nassar and Martin Crompton (Al-Nasser and Crompton 1986) presented evidence that the previously reported mitochondrial swelling and dysfunction caused by high Ca2+ are due to reversible permeabilization of the mitochondria.