Autophagy in major human diseases
Daniel J. Klionsky, Giulia Petroni, Ravi K. Amaravadi, Eric H. Baehrecke, Andrea Ballabio, Patricia Boya, José Manuel Bravo‐San Pedro, Ken Cadwell, Francesco Cecconi, Augustine M.K. Choi, Mary E. Choi, Charleen T. Chu, Patrice Codogno, María Isabel Colombo, Ana María Cuervo, Vojo Deretić, Ivan Đikić, Zvulun Elazar, Eeva‐Liisa Eskelinen, Gian María Fimia, David A. Gewirtz, Douglas R. Green, Malene Hansen, Marja Jäättelä, Terje Johansen, Gábor Juhász, Vassiliki Karantza, Claudine Kraft, Guido Kroemer, Nicholas T. Ktistakis, Sharad Kumar, Carlos López-Otı́n, Kay F. Macleod, Frank Madeo, Jennifer Martinez, Alicia Meléndez, Noboru Mizushima, Christian Münz, Josef Penninger, Rushika M. Perera, Mauro Piacentini, Fulvio Reggiori, David C. Rubinsztein, Kevin M. Ryan, Junichi Sadoshima, Laura Santambrogio, Luca Scorrano, Hans‐Uwe Simon, Anna Katharina Simon, Anne Simonsen, Alexandra Stolz, Nektarios Tavernarakis, Sharon A. Tooze, Tamotsu Yoshimori, Junying Yuan, Zhenyu Yue, Qing Zhong, Lorenzo Galluzzi, Federico Pietrocola
Abstract
Autophagy is a core molecular pathway for the preservation of cellular and organismal homeostasis. Pharmacological and genetic interventions impairing autophagy responses promote or aggravate disease in a plethora of experimental models. Consistently, mutations in autophagy-related processes cause severe human pathologies. Here, we review and discuss preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.