Apoptosis in Cardiac Biology by Jürgen Holtz M.D., Dorothea Darmer Ph.D. (auth.), Heribert PDF

By Jürgen Holtz M.D., Dorothea Darmer Ph.D. (auth.), Heribert Schunkert, G. A. J. Riegger (eds.)

ISBN-10: 0585381437

ISBN-13: 9780585381435

ISBN-10: 0792386485

ISBN-13: 9780792386483

Apoptosis or programmed telephone demise is more and more thought of to be a significant component within the improvement and development of heart problems. In sufferers with center failure the activation of apoptosis can result within the lack of irreplaceable cardiac myocytes selling the scientific process the syndrome. in addition, within the coronary arteries irritation and apoptosis might weaken severe buildings of the vessel wall resulting in plaque rupture and, therefore, to myocardial infarction. Given those deleterious results, it kind of feels nearly paradoxical that programmed telephone dying is an lively technique that, if initiated below physiological conditions, is vital for either coordinated tissue development or destruction of malignant cells.
Apoptosis in Cardiac Biology, written by means of a group of across the world popular researchers, offers a well timed synopsis of easy mechanisms, mobile and structural objectives and, eventually, scientific implications of programmed telephone loss of life within the center. The specialist authors of this quantity provide concise overviews on normal and cell-specific elements of programmed cellphone dying in cardiac myocytes and fibroblasts, in addition to in vascular delicate muscle and endothelial cells. additionally, novel healing recommendations bobbing up from the phenomenal pathophysiological importance of cardiac apoptosis are offered.
This complete assessment of Apoptosis in Cardiac Biology might be of curiosity to either clinicians and easy researchers who're energetic within the fields of cardiology and atherosclerosis.

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M. Debatin, P. H. Krammer, and M. E. Peter. Two CD95 (APO-1lFas) signaling pathways. EMBO J 17: 1675-1687, 1998. APOPTOSIS IN CARDIAC BIOLOGY Schall, T. , M. Lewis, K. J. Koller, A. Lee, G. C. Rice, G. H. W. Wong, T. Gatanaga, G. A. Granger, R. Lentz, H. Raab, W. J. Kohr, and D. V. Goeddel. Molecular cloning and expression of a receptor for human tumor necrosis factor. Cell 61: 361-370, 1990. , J. L. Bodmer, M. Thome, K. Hofmann, N. Holler, and J. Tschopp. Characterization of two receptors for TRAIL.

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Stabilization of functional tumor necrosis factor-a by its soluble TNF receptors. Eur Cytokine Nem 4: 359-362, 1993. , V. Goossens, E. Boone, D. Vercammen, K, Vancompernolle, P. Vandenabeele, G. Haegeman, W. Fiers, and J. Grooten. The 55-kDa tumor necrosis factor receptor induces clustering of mitochondria through its membrane-proximal region. J B i d Chem 273: 9673-9680, 1998. , S. Geley, R. Hirsch, M. Castedo, P. Marchetti, A. Macho, R. Kofler, and G. Kroemer. Bcl-2 and Bcl-xL antagonize the mitochondria1 dysfunction preceding nuclear apoptosis induced by chemotherapeutic agents.

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Apoptosis in Cardiac Biology by Jürgen Holtz M.D., Dorothea Darmer Ph.D. (auth.), Heribert Schunkert, G. A. J. Riegger (eds.)

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