Klionsky DJ., Petroni G., Amaravadi RK., Baehrecke EH., Ballabio A., Boya P., Bravo-San Pedro JM., Cadwell K., Cecconi F., Choi AMK., Choi ME., Chu CT., Codogno P., Colombo MI., Cuervo AM., Deretic V., Dikic I., Elazar Z., Eskelinen E-L., Fimia GM., Gewirtz DA., Green DR., Hansen M., Jäättelä M., Johansen T., Juhász G., Karantza V., Kraft C., Kroemer G., Ktistakis NT., Kumar S., Lopez-Otin C., Macleod KF., Madeo F., Martinez J., Meléndez A., Mizushima N., Münz C., Penninger JM., Perera RM., Piacentini M., Reggiori F., Rubinsztein DC., Ryan KM., Sadoshima J., Santambrogio L., Scorrano L., Simon H-U., Simon AK., Simonsen A., Stolz A., Tavernarakis N., Tooze SA., Yoshimori T., Yuan J., Yue Z., Zhong Q., Galluzzi L., Pietrocola F.

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.

phagy in major human diseases.

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