Free Access
Med Sci (Paris)
Volume 33, Number 3, Mars 2017
Page(s) 290 - 296
Section M/S Revues
Published online 03 April 2017
  1. Barker N. Adult intestinal stem cells: critical drivers of epithelial homeostasis and regeneration. Nat Rev Mol Cell Biol 2014 ; 15 : 19–33. [CrossRef] [PubMed] [Google Scholar]
  2. Vaishnava S, Behrendt CL, Ismail AS, et al. Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface. Proc Natl Acad Sci USA 2008 ; 105 : 20858–20863. [CrossRef] [Google Scholar]
  3. Stappenbeck TS The role of autophagy in Paneth cell differentiation and secretion. Mucosal Immunol 2010 ; 3 : 8–10. [Google Scholar]
  4. Cadwell K, Liu JY, Brown SL, et al. A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells. Nature 2008 ; 456 : 259–263. [CrossRef] [PubMed] [Google Scholar]
  5. Cadwell K, Patel KK, Maloney NS, et al. Virus-plus-susceptibility gene interaction determines Crohn’s disease gene Atg16L1 phenotypes in intestine. Cell 2010 ; 141 : 1135–1145. [CrossRef] [PubMed] [Google Scholar]
  6. Patel KK, Miyoshi H, Beatty WL, et al. Autophagy proteins control goblet cell function by potentiating reactive oxygen species production. EMBO J 2013 ; 32 : 3130–3144. [CrossRef] [PubMed] [Google Scholar]
  7. Lassen KG, Kuballa P, Conway KL, et al. Atg16L1 T300A variant decreases selective autophagy resulting in altered cytokine signaling and decreased antibacterial defense. Proc Natl Acad Sci USA 2014 ; 111 : 7741–7746. [CrossRef] [Google Scholar]
  8. Levy J, Romagnolo B Autophagy, microbiota and intestinal oncogenesis. Oncotarget 2015 ; 6 : 34067–34068. [CrossRef] [PubMed] [Google Scholar]
  9. Tsuboi K, Nishitani M, Takakura A, et al. Autophagy protects against colitis by the maintenance of normal gut microflora and secretion of mucus. J Biol Chem 2015 ; 290 : 20511–20526. [CrossRef] [PubMed] [Google Scholar]
  10. Adolph TE, Tomczak MF, Niederreiter L, et al. Paneth cells as a site of origin for intestinal inflammation. Nature 2013 ; 503 : 272–276. [CrossRef] [PubMed] [Google Scholar]
  11. Levy J, Cacheux W, Bara MA, et al. Intestinal inhibition of Atg7 prevents tumour initiation through a microbiome-influenced immune response and suppresses tumour growth. Nat Cell Biol 2015 ; 17 : 1062–1073. [CrossRef] [PubMed] [Google Scholar]
  12. Sadaghian Sadabad M, Regeling A, de Goffau MC, et al. The ATG16L1-T300A allele impairs clearance of pathosymbionts in the inflamed ileal mucosa of Crohn’s disease patients. Gut 2015 ; 64 : 1546–1552. [CrossRef] [PubMed] [Google Scholar]
  13. Benjamin JL, Sumpter R, Jr., Levine B, Hooper LV Intestinal epithelial autophagy is essential for host defense against invasive bacteria. Cell Host Microbe 2013 ; 13 : 723–734. [CrossRef] [PubMed] [Google Scholar]
  14. Chang SY, Lee SN, Yang JY, et al. Autophagy controls an intrinsic host defense to bacteria by promoting epithelial cell survival: a murine model. PLoS One 2013 ; 8 : e81095. [CrossRef] [PubMed] [Google Scholar]
  15. Conway KL, Kuballa P, Song JH, et al. Atg16l1 is required for autophagy in intestinal epithelial cells and protection of mice from Salmonella infection. Gastroenterology 2013 ; 145 : 1347–1357. [CrossRef] [PubMed] [Google Scholar]
  16. Mimouna S, Bazin M, Mograbi B, et al. HIF1A regulates xenophagic degradation of adherent and invasive Escherichia coli (AIEC). Autophagy 2014 ; 10 : 2333–2345. [CrossRef] [PubMed] [Google Scholar]
  17. Yilmaz OH, Katajisto P, Lamming DW, et al. mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake. Nature 2012 ; 486 : 490–495. [CrossRef] [PubMed] [Google Scholar]
  18. Igarashi M, Guarente L mTORC1 and SIRT1 cooperate to foster expansion of gut adult stem cells during calorie restriction. Cell 2016 ; 166 : 436–450. [CrossRef] [PubMed] [Google Scholar]
  19. Durand A, Donahue B, Peignon G, et al. Functional intestinal stem cells after Paneth cell ablation induced by the loss of transcription factor Math1 (Atoh1). Proc Natl Acad Sci USA 2012 ; 109 : 8965–8970. [CrossRef] [Google Scholar]
  20. Sato T, van Es JH, Snippert HJ, et al. Paneth cells constitute the niche for Lgr5 stem cells in intestinal crypts. Nature 2011 ; 469 : 415–418. [CrossRef] [PubMed] [Google Scholar]
  21. Galluzzi L, Pietrocola F, Levine B, Kroemer G Metabolic control of autophagy. Cell 2014 ; 159 : 1263–1276. [CrossRef] [PubMed] [Google Scholar]
  22. Ravindran R, Loebbermann J, Nakaya HI, et al. The amino acid sensor GCN2 controls gut inflammation by inhibiting inflammasome activation. Nature 2016 ; 531 : 523–527. [CrossRef] [PubMed] [Google Scholar]
  23. Fontana L, Partridge L Promoting health and longevity through diet: from model organisms to humans. Cell 2015 ; 161 : 106–118. [CrossRef] [PubMed] [Google Scholar]
  24. Madeo F, Zimmermann A, Maiuri MC, Kroemer G Essential role for autophagy in life span extension. J Clin Invest 2015 ; 125 : 85–93. [CrossRef] [PubMed] [Google Scholar]
  25. Gelino S, Chang JT, Kumsta C, et al. Intestinal autophagy improves healthspan and longevity in C. elegans during dietary restriction. PLoS Genet 2016 ; 12 : e1006135. [CrossRef] [PubMed] [Google Scholar]
  26. Rera M, Clark RI, Walker DW Intestinal barrier dysfunction links metabolic and inflammatory markers of aging to death in Drosophila. Proc Natl Acad Sci USA 2012 ; 109 : 21528–21533. [CrossRef] [Google Scholar]
  27. Guo L, Karpac J, Tran SL, Jasper H PGRP-SC2 promotes gut immune homeostasis to limit commensal dysbiosis and extend lifespan. Cell 2014 ; 156 : 109–122. [CrossRef] [PubMed] [Google Scholar]
  28. Clark RI, Salazar A, Yamada R, et al. Distinct shifts in microbiota composition during Drosophila aging impair intestinal function and drive mortality. Cell Rep 2015 ; 12 : 1656–1667. [CrossRef] [PubMed] [Google Scholar]
  29. Rioux JD, Xavier RJ, Taylor KD, et al. Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis. Nat Genet 2007 ; 39 : 596–604. [Google Scholar]
  30. Murthy A, Li Y, Peng I, et al. A Crohn’s disease variant in Atg16l1 enhances its degradation by caspase 3. Nature 2014 ; 506 : 456–462. [CrossRef] [PubMed] [Google Scholar]
  31. Brest P, Lapaquette P, Souidi M, et al. A synonymous variant in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn’s disease. Nat Genet 2011 ; 43 : 242–245. [Google Scholar]
  32. Hampe J, Cuthbert A, Croucher PJ, et al. Association between insertion mutation in NOD2 gene and Crohn’s disease in German and British populations. Lancet 2001 ; 357 : 1925–1928. [CrossRef] [PubMed] [Google Scholar]
  33. Travassos LH, Carneiro LA, Ramjeet M, et al. Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. Nat Immunol 2010 ; 11 : 55–62. [CrossRef] [PubMed] [Google Scholar]
  34. Cooney R, Baker J, Brain O, et al. NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation. Nat Med 2010 ; 16 : 90–97. [CrossRef] [PubMed] [Google Scholar]
  35. Chauhan S, Mandell MA, Deretic V IRGM governs the core autophagy machinery to conduct antimicrobial defense. Mol Cell 2015 ; 58 : 507–521. [CrossRef] [PubMed] [Google Scholar]
  36. Liu B, Gulati AS, Cantillana V, et al. Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation. Am J Physiol Gastrointest Liver Physiol 2013 ; 305 : G573–G584. [CrossRef] [PubMed] [Google Scholar]
  37. Miao Y, Zhang Y, Chen Y, et al. GABARAP is overexpressed in colorectal carcinoma and correlates with shortened patient survival. Hepatogastroenterology 2010 ; 57 : 257–261. [PubMed] [Google Scholar]
  38. Zou Y, Chen Z, He X, et al. High expression levels of unc-51-like kinase 1 as a predictor of poor prognosis in colorectal cancer. Oncol Lett 2015 ; 10 : 1583–1588. [CrossRef] [PubMed] [Google Scholar]
  39. Schmitz KJ, Ademi C, Bertram S, et al. Prognostic relevance of autophagy-related markers LC3, p62/sequestosome 1, Beclin-1 and ULK1 in colorectal cancer patients with respect to KRAS mutational status. World J Surg Oncol 2016 ; 14 : 189. [CrossRef] [PubMed] [Google Scholar]
  40. Guo GF, Jiang WQ, Zhang B, et al. Autophagy-related proteins Beclin-1 and LC3 predict cetuximab efficacy in advanced colorectal cancer. World J Gastroenterol 2011 ; 17 : 4779–4786. [CrossRef] [PubMed] [Google Scholar]
  41. Park JM, Huang S, Wu TT, et al. Prognostic impact of Beclin 1, p62/sequestosome 1 and LC3 protein expression in colon carcinomas from patients receiving 5-fluorouracil as adjuvant chemotherapy. Cancer Biol Ther 2013 ; 14 : 100–107. [CrossRef] [PubMed] [Google Scholar]
  42. Guo JY, Chen HY, Mathew R, et al. Activated Ras requires autophagy to maintain oxidative metabolism and tumorigenesis. Genes Dev 2011 ; 25 : 460–470. [CrossRef] [PubMed] [Google Scholar]
  43. Rao S, Tortola L, Perlot T, et al. A dual role for autophagy in a murine model of lung cancer. Nat Commun 2014 ; 5 : 3056. [PubMed] [Google Scholar]
  44. Rosenfeldt MT, O’Prey J, Morton JP, et al. p53 status determines the role of autophagy in pancreatic tumour development. Nature 2013 ; 504 : 296–300. [CrossRef] [PubMed] [Google Scholar]
  45. Sakitani K, Hirata Y, Hikiba Y, et al. Inhibition of autophagy exerts anti-colon cancer effects via apoptosis induced by p53 activation and ER stress. BMC Cancer 2015 ; 15 : 795. [CrossRef] [PubMed] [Google Scholar]
  46. Grimm WA, Messer JS, Murphy SF, et al. The Thr300Ala variant in ATG16L1 is associated with improved survival in human colorectal cancer and enhanced production of type I interferon. Gut 2015 ; 65 : 456–464. [CrossRef] [PubMed] [Google Scholar]

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