TY - JOUR
T1 - Biological Functions of Autophagy Genes
T2 - A Disease Perspective
AU - Levine, Beth
AU - Kroemer, Guido
N1 - Funding Information:
The authors thank H. Smith for assistance with manuscript preparation and A. Diehl for expert medical illustration. The work in the authors’ laboratories was supported by NIH grants RO1 CA109618 and U19 AI109725 (B.L.), Cancer Prevention Research Institute of Texas (CPRIT) grant RP120718 (B.L.), and Fondation Leducq grant 15CBD04 (B.L., G.K.). G.K. was supported by Ligue contre le Cancer (équipe labelisée); Agence National de la Recherche (ANR) – Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; Association pour la recherche sur le cancer (ARC); Cancéropôle Ile-de-France ; Chancelerie des universités de Paris (Legs Poix); Fondation pour la Recherche Médicale (FRM); European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); the European Research Council (ERC); Fondation Carrefour ; Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France ; the LabEx Immuno-Oncology ; the RHU Torino Lumière ; the Seerave Foundation ; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); and the SIRIC Cancer Research and Personalized Medicine (CARPEM). We apologize to all those authors whose work could not be cited due to space limitations.
Funding Information:
The authors thank H. Smith for assistance with manuscript preparation and A. Diehl for expert medical illustration. The work in the authors’ laboratories was supported by NIH grants RO1 CA109618 and U19 AI109725 (B.L.), Cancer Prevention Research Institute of Texas (CPRIT) grant RP120718 (B.L.), and Fondation Leducq grant 15CBD04 (B.L., G.K.). G.K. was supported by Ligue contre le Cancer (équipe labelisée); Agence National de la Recherche (ANR) – Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; Association pour la recherche sur le cancer (ARC); Cancéropôle Ile-de-France; Chancelerie des universités de Paris (Legs Poix); Fondation pour la Recherche Médicale (FRM); European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); the European Research Council (ERC); Fondation Carrefour; Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France; the LabEx Immuno-Oncology; the RHU Torino Lumière; the Seerave Foundation; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); and the SIRIC Cancer Research and Personalized Medicine (CARPEM). We apologize to all those authors whose work could not be cited due to space limitations.
Funding Information:
The authors thank H. Smith for assistance with manuscript preparation and A. Diehl for expert medical illustration. The work in the authors? laboratories was supported by NIH grants RO1 CA109618 and U19 AI109725 (B.L.), Cancer Prevention Research Institute of Texas (CPRIT) grant RP120718 (B.L.), and Fondation Leducq grant 15CBD04 (B.L., G.K.). G.K. was supported by Ligue contre le Cancer (?quipe labelis?e); Agence National de la Recherche (ANR) ? Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; Association pour la recherche sur le cancer (ARC); Canc?rop?le Ile-de-France; Chancelerie des universit?s de Paris (Legs Poix); Fondation pour la Recherche M?dicale (FRM); European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); the European Research Council (ERC); Fondation Carrefour; Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France; the LabEx Immuno-Oncology; the RHU Torino Lumi?re; the Seerave Foundation; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); and the SIRIC Cancer Research and Personalized Medicine (CARPEM). We apologize to all those authors whose work could not be cited due to space limitations.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2019/1/10
Y1 - 2019/1/10
N2 - The lysosomal degradation pathway of autophagy plays a fundamental role in cellular, tissue, and organismal homeostasis and is mediated by evolutionarily conserved autophagy-related (ATG) genes. Definitive etiological links exist between mutations in genes that control autophagy and human disease, especially neurodegenerative, inflammatory disorders and cancer. Autophagy selectively targets dysfunctional organelles, intracellular microbes, and pathogenic proteins, and deficiencies in these processes may lead to disease. Moreover, ATG genes have diverse physiologically important roles in other membrane-trafficking and signaling pathways. This Review discusses the biological functions of autophagy genes from the perspective of understanding—and potentially reversing—the pathophysiology of human disease and aging.
AB - The lysosomal degradation pathway of autophagy plays a fundamental role in cellular, tissue, and organismal homeostasis and is mediated by evolutionarily conserved autophagy-related (ATG) genes. Definitive etiological links exist between mutations in genes that control autophagy and human disease, especially neurodegenerative, inflammatory disorders and cancer. Autophagy selectively targets dysfunctional organelles, intracellular microbes, and pathogenic proteins, and deficiencies in these processes may lead to disease. Moreover, ATG genes have diverse physiologically important roles in other membrane-trafficking and signaling pathways. This Review discusses the biological functions of autophagy genes from the perspective of understanding—and potentially reversing—the pathophysiology of human disease and aging.
UR - http://www.scopus.com/inward/record.url?scp=85059392998&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85059392998&partnerID=8YFLogxK
U2 - 10.1016/j.cell.2018.09.048
DO - 10.1016/j.cell.2018.09.048
M3 - Review article
C2 - 30633901
AN - SCOPUS:85059392998
SN - 0092-8674
VL - 176
SP - 11
EP - 42
JO - Cell
JF - Cell
IS - 1-2
ER -