By Roberta A. Gottlieb
Autophagy in wellbeing and fitness and Disease bargains an outline of the newest learn in autophagy with a translational emphasis. This ebook takes medical learn in autophagy a step extra and gives built-in content material with developments in autophagy from cellphone biology and biochemical examine to medical remedies. an important reference for the bookshelf of clinical and clinical researchers and scholars, Autophagy in healthiness and Disease provides top of the range, respected details on autophagy, permitting the reader easy accessibility to the main appropriate information.
- Discusses present knowing of the jobs of autophagy in future health and disease
- Covers the historical past of autophagy, the improvement of instruments and therapeutics to degree and modulate autophagy, and autophagy in tissues and sickness processes
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Additional info for Autophagy in Health and Disease
Wang ZV, Rothermel BA, Hill JA. Autophagy in hypertensive heart disease. J Biol Chem 2010;285:8509e14. 30. Yamamoto S, Sawada K, Shimomura H, Kawamura K, James TN. On the nature of cell death during remodeling of hypertrophied human myocardium. J Mol Cell Cardiol 2000;32:161e75. 31. Pfeifer U, Fohr J, Wilhelm W, Dammrich J. Short-term inhibition of cardiac cellular autophagy by isoproterenol. J Mol Cell Cardiol 1987;19:1179e84. 32. Imamura T, McDermott PJ, Kent RL, Nagatsu M, Gt Cooper, Carabello BA.
McMullen JR, Sherwood MC, Tarnavski O, Zhang L, Dorfman AL, Shioi T, et al. Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload. Circulation 2004;109:3050e5. 37. Zhu H, Tannous P, Johnstone JL, Kong Y, Shelton JM, Richardson JA, et al. Cardiac autophagy is a maladaptive response to hemodynamic stress. J Clin Invest 2007;117:1782e93. 38. Knaapen MW, Davies MJ, De Bie M, Haven AJ, Martinet W, Kockx MM. Apoptotic versus autophagic cell death in heart failure.
Hubbard et al showed that cytokine production and proliferation of Th cells after engagement of the TCR and the CD28 costimulatory molecule requires autophagosome formation and clearance33. Using a conditional knockout mouse model in which Atg7 is specifically deleted in T cells, effector Th cells display defective IL-2 and Interferon-g (IFN-g) production, reduced proliferation, with no significant increase in apoptosis and a decline in ATP generation. Importantly, when an exogenous energy source was provided to the Atg7 deleted Th cells, cytokine production was restored.