Autophagy: a lysosomal degradation pathway with a central role in health and disease

Biochimica Et Biophysica Acta
Eeva-Liisa Eskelinen, Paul Saftig

Abstract

Autophagy delivers cytoplasmic material and organelles to lysosomes for degradation. The formation of autophagosomes is controlled by a specific set of autophagy genes called atg genes. The magnitude of autophagosome formation is tightly regulated by intracellular and extracellular amino acid concentrations and ATP levels via signaling pathways that include the nutrient sensing kinase TOR. Autophagy functions as a stress response that is upregulated by starvation, oxidative stress, or other harmful conditions. Remarkably, autophagy has been shown to possess important housekeeping and quality control functions that contribute to health and longevity. Autophagy plays a role in innate and adaptive immunity, programmed cell death, as well as prevention of cancer, neurodegeneration and aging. In addition, impaired autophagic degradation contributes to the pathogenesis of several human diseases including lysosomal storage disorders and muscle diseases.

References

Apr 15, 1992·The Biochemical Journal·P B GordonP O Seglen
Jan 1, 1990·Virchows Archiv. B, Cell Pathology Including Molecular Pathology·N Jurilj, U Pfeifer
Feb 3, 1995·The Journal of Biological Chemistry·E F BlommaartA J Meijer
Jan 13, 1997·The Journal of Cell Biology·W LiouJ W Slot
Sep 20, 2000·The Journal of Cell Biology·Y KamadaY Ohsumi
Mar 27, 2001·Nature Reviews. Molecular Cell Biology·Y Ohsumi
Mar 27, 2001·The Journal of Cell Biology·N MizushimaT Yoshimori
Sep 6, 2001·Cell Death and Differentiation·W Bursch
Jan 5, 2002·Proceedings of the National Academy of Sciences of the United States of America·Zsolt TallóczyBeth Levine
Apr 9, 2002·Cell Structure and Function·Atsuki NaraTamotsu Yoshimori
Sep 11, 2002·Molecular Biology of the Cell·Eeva-Liisa EskelinenPaul Saftig
Nov 28, 2002·Traffic·Eeva-Liisa EskelinenJohn M Lucocq
Jan 1, 2003·Current Neurology and Neuroscience Reports·Ichizo Nishino
Mar 26, 2003·Cell Structure and Function·Maho HamasakiYoshinori Ohsumi
Jun 20, 2003·Cellular Microbiology·Kathryn A RichPaul Webster
Oct 11, 2003·Developmental Cell·Daniel J KlionskyYoshinori Ohsumi
Nov 26, 2003·The Journal of Clinical Investigation·Xueping QuBeth Levine
Dec 6, 2003·Proceedings of the National Academy of Sciences of the United States of America·Zhenyu YueNathaniel Heintz
Dec 20, 2003·Biochemical and Biophysical Research Communications·Alfred J Meijer, Peter F Dubbelhuis
May 4, 2004·Molecular Biology of the Cell·Eeva-Liisa EskelinenPaul Saftig

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Citations

Dec 24, 2011·European Journal of Applied Physiology·Cécile JamartMarc Francaux
Aug 27, 2009·Journal of Neural Transmission·Kurt A Jellinger
Apr 30, 2010·Journal of Inherited Metabolic Disease·Cinzia Maria Bellettato, Maurizio Scarpa
Jul 10, 2012·Journal of Inherited Metabolic Disease·Louise D ArcherJames E Fildes
May 9, 2013·Journal of Inherited Metabolic Disease·Louise D ArcherJames E Fildes
Dec 30, 2011·Journal of Physiology and Biochemistry·Yong An KimWook Song
Mar 9, 2013·Journal of Physiology and Biochemistry·Yong An KimWook Song
Jun 1, 2012·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Weipei ZhuXueguan Lu
Feb 5, 2011·Cell Death and Differentiation·Q RemijsenT Vanden Berghe
Dec 31, 2009·Antioxidants & Redox Signaling·Tino KurzUlf T Brunk
Aug 18, 2010·Antioxidants & Redox Signaling·Isei Tanida
Mar 1, 2012·The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences·Maria I BehrensAndrew F G Quest
Dec 15, 2011·Cold Spring Harbor Perspectives in Biology·Li Yen Mah, Kevin M Ryan
Nov 5, 2010·Diabetes, Obesity & Metabolism·G Las, O S Shirihai
Sep 11, 2012·American Journal of Physiology. Gastrointestinal and Liver Physiology·Anna S Gukovskaya, Ilya Gukovsky
Dec 1, 2012·American Journal of Physiology. Renal Physiology·Nirmala Parajuli, Lee Ann MacMillan-Crow
Oct 31, 2012·Obesity Facts·Nitzan MaixnerAssaf Rudich
Mar 23, 2010·Biological Chemistry·Nadja KetternJörg Höhfeld
Jun 2, 2012·Frontiers in Bioscience (Scholar Edition)·Rodney J Devenish, Daniel J Klionsky
Nov 30, 2013·BioMed Research International·Tamotsu TsukaharaHisao Haniu
May 1, 2013·EMBO Molecular Medicine·Ivan NemazanyyGanna Panasyuk
Jan 28, 2014·Pharmacology & Therapeutics·Karina HuynhRebecca H Ritchie
Dec 18, 2013·Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban·Zhong-qiang WangQiu-hong Duan
Dec 27, 2013·Experimental and Molecular Pathology·Lili BaoSrikanta Dash
Mar 19, 2014·International Journal of Cell Biology·Stefan W RyterAugustine M K Choi
Jun 20, 2014·British Journal of Cancer·S SumanC Damodaran
Jun 24, 2014·Rejuvenation Research·Ben A Bahr
Jan 15, 2014·Journal of Molecular Neuroscience : MN·Qiaoyu SunLili Zhang

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