Open Access
Issue
Med Sci (Paris)
Volume 36, Number 2, Février 2020
Page(s) 119 - 129
Section M/S Revues
DOI https://doi.org/10.1051/medsci/2020008
Published online 04 March 2020
  1. Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016 ; 64 : 73–84. [CrossRef] [PubMed] [Google Scholar]
  2. Piscaglia F, Svegliati-Baroni G, Barchetti A, et al. Clinical patterns of hepatocellular carcinoma in nonalcoholic fatty liver disease: a multicenter prospective study. Hepatology 2016 ; 63 : 827–838. [CrossRef] [PubMed] [Google Scholar]
  3. Arrese M, Cabrera D, Kalergis AM, Feldstein AE. Innate Immunity and Inflammation in NAFLD/NASH. Dig Dis Sci 2016 ; 61 : 1294–1303. [CrossRef] [PubMed] [Google Scholar]
  4. Lebeaupin C, Vallee D, Hazari Y, et al. Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. J Hepatol 2018 ; 69 : 927–947. [CrossRef] [PubMed] [Google Scholar]
  5. Bouchecareilh M, Chevet E. Stress du réticulum endoplasmique : une réponse pour éviter le pIRE. Med Sci (Paris) 2009 ; 25 : 281–287. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  6. Cullinan SB, Diehl JA. PERK-dependent activation of Nrf2 contributes to redox homeostasis and cell survival following endoplasmic reticulum stress. J Biol Chem 2004 ; 279 : 20108–20117. [CrossRef] [PubMed] [Google Scholar]
  7. Harding HP, Zhang Y, Zeng H, et al. An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. Mol Cell 2003 ; 11 : 619–633. [CrossRef] [PubMed] [Google Scholar]
  8. Adachi Y, Yamamoto K, Okada T, et al. ATF6 is a transcription factor specializing in the regulation of quality control proteins in the endoplasmic reticulum. Cell Struct Funct 2008 ; 33 : 75–89. [CrossRef] [PubMed] [Google Scholar]
  9. Yamamoto K, Takahara K, Oyadomari S, et al. Induction of liver steatosis and lipid droplet formation in ATF6alpha-knockout mice burdened with pharmacological endoplasmic reticulum stress. Mol Biol Cell 2010 ; 21 : 2975–2986. [CrossRef] [PubMed] [Google Scholar]
  10. Wang JM, Qiu Y, Yang Z, et al. IRE1alpha prevents hepatic steatosis by processing and promoting the degradation of select microRNAs. Sci Signal 2018 ; 11 : [Google Scholar]
  11. Foufelle F, Ferre P. La réponse UPR : son rôle physiologique et physiopathologique. Med Sci (Paris) 2007 ; 23 : 291–296. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  12. Ozcan U, Cao Q, Yilmaz E, et al. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science 2004 ; 306 : 457–461. [Google Scholar]
  13. Gregor MF, Yang L, Fabbrini E, et al. Endoplasmic reticulum stress is reduced in tissues of obese subjects after weight loss. Diabetes 2009 ; 58 : 693–700. [CrossRef] [PubMed] [Google Scholar]
  14. Lake AD, Novak P, Hardwick RN, et al. The adaptive endoplasmic reticulum stress response to lipotoxicity in progressive human nonalcoholic fatty liver disease. Toxicol Sci 2014 ; 137 : 26–35. [CrossRef] [PubMed] [Google Scholar]
  15. Yoshiuchi K, Kaneto H, Matsuoka TA, et al. Direct monitoring of in vivo ER stress during the development of insulin resistance with ER stress-activated indicator transgenic mice. Biochem Biophys Res Commun 2008 ; 366 : 545–550. [Google Scholar]
  16. Kammoun HL, Chabanon H, Hainault I, et al. GRP78 expression inhibits insulin and ER stress-induced SREBP-1c activation and reduces hepatic steatosis in mice. J Clin Invest 2009 ; 119 : 1201–1215. [CrossRef] [PubMed] [Google Scholar]
  17. Gorden DL, Myers DS, Ivanova PT, et al. Biomarkers of NAFLD progression: a lipidomics approach to an epidemic. J Lipid Res 2015 ; 56 : 722–736. [CrossRef] [PubMed] [Google Scholar]
  18. Farese RV, Jr., Zechner R, Newgard CB, Walther TC. The problem of establishing relationships between hepatic steatosis and hepatic insulin resistance. Cell Metab 2012 ; 15 : 570–573. [CrossRef] [PubMed] [Google Scholar]
  19. Flamment M, Foufelle F. Stéatose hépatique et stress du réticulum endoplasmique : une histoire de phospholipides. Med Sci (Paris) 2012 ; 28 : 13–15. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]
  20. Volmer R, van der Ploeg K, Ron D. Membrane lipid saturation activates endoplasmic reticulum unfolded protein response transducers through their transmembrane domains. Proc Natl Acad Sci USA 2013 ; 110 : 4628–4633. [CrossRef] [Google Scholar]
  21. Patterson RE, Kalavalapalli S, Williams CM, et al. Lipotoxicity in steatohepatitis occurs despite an increase in tricarboxylic acid cycle activity. Am J Physiol Endocrinol Metab 2016 ; 310 : E484–E494. [CrossRef] [PubMed] [Google Scholar]
  22. Patouraux S, Rousseau D, Bonnafous S, et al. CD44 is a key player in non-alcoholic steatohepatitis. J Hepatol 2017 ; 67 : 328–338. [CrossRef] [PubMed] [Google Scholar]
  23. Feldstein AE, Canbay A, Angulo P, et al. Hepatocyte apoptosis and fas expression are prominent features of human nonalcoholic steatohepatitis. Gastroenterology 2003 ; 125 : 437–443. [CrossRef] [PubMed] [Google Scholar]
  24. Deng J, Lu PD, Zhang Y, et al. Translational repression mediates activation of nuclear factor kappa B by phosphorylated translation initiation factor 2. Mol Cell Biol 2004 ; 24 : 10161–10168. [CrossRef] [PubMed] [Google Scholar]
  25. Luedde T, Schwabe RF. NF-kappaB in the liver: linking injury, fibrosis and hepatocellular carcinoma. Nat Rev Gastroenterol Hepatol 2011 ; 8 : 108–118. [CrossRef] [PubMed] [Google Scholar]
  26. Willy JA, Young SK, Stevens JL, et al. CHOP links endoplasmic reticulum stress to NF-kappaB activation in the pathogenesis of nonalcoholic steatohepatitis. Mol Biol Cell 2015 ; 26 : 2190–2204. [CrossRef] [PubMed] [Google Scholar]
  27. Yoneda M, Mawatari H, Fujita K, et al. High-sensitivity C-reactive protein is an independent clinical feature of nonalcoholic steatohepatitis (NASH) and also of the severity of fibrosis in NASH. J Gastroenterol 2007 ; 42 : 573–582. [CrossRef] [PubMed] [Google Scholar]
  28. Lebeaupin C, Proics E, de Bieville CH, et al. ER stress induces NLRP3 inflammasome activation and hepatocyte death. Cell Death Dis 2015 ; 6 : e1879. [CrossRef] [PubMed] [Google Scholar]
  29. Stienstra R, van Diepen JA, Tack CJ, et al. Inflammasome is a central player in the induction of obesity and insulin resistance. Proc Natl Acad Sci USA 2011 ; 108 : 15324–15329. [CrossRef] [Google Scholar]
  30. Galluzzi L, Vitale I, Abrams JM, et al. Molecular definitions of cell death subroutines: recommendations of the nomenclature committee on cell death 2012. Cell Death Differ 2012 ; 19 : 107–120. [CrossRef] [PubMed] [Google Scholar]
  31. Wree A, Eguchi A, McGeough MD, et al. NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation, and fibrosis in mice. Hepatology 2014 ; 59 : 898–910. [CrossRef] [PubMed] [Google Scholar]
  32. Mridha AR, Wree A, Robertson AAB, et al. NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice. J Hepatol 2017 ; 66 : 1037–1046. [CrossRef] [PubMed] [Google Scholar]
  33. Lerner AG, Upton JP, Praveen PV, et al. IRE1alpha induces thioredoxin-interacting protein to activate the NLRP3 inflammasome and promote programmed cell death under irremediable ER stress. Cell Metab 2012 ; 16 : 250–264. [CrossRef] [PubMed] [Google Scholar]
  34. Lebeaupin C, Vallee D, Rousseau D, et al. Bax inhibitor-1 protects from nonalcoholic steatohepatitis by limiting inositol-requiring enzyme 1 alpha signaling in mice. Hepatology 2018 ; 68 : 515–532. [CrossRef] [PubMed] [Google Scholar]
  35. Zmijewski JW, Banerjee S, Bae H, et al. Exposure to hydrogen peroxide induces oxidation and activation of AMP-activated protein kinase. J Biol Chem 2010 ; 285 : 33154–33164. [CrossRef] [PubMed] [Google Scholar]
  36. Okada K, Warabi E, Sugimoto H, et al. Nrf2 inhibits hepatic iron accumulation and counteracts oxidative stress-induced liver injury in nutritional steatohepatitis. J Gastroenterol 2012 ; 47 : 924–935. [CrossRef] [PubMed] [Google Scholar]
  37. Shan B, Wang X, Wu Y, et al. The metabolic ER stress sensor IRE1alpha suppresses alternative activation of macrophages and impairs energy expenditure in obesity. Nat Immunol 2017 ; 18 : 519–529. [CrossRef] [PubMed] [Google Scholar]
  38. Reverendo M, Mendes A, Argüello RJ, et al. At the crossway of ER-stress and proinflammatory responses. The FEBS Journal 2019 ; 286 : 297–310. [CrossRef] [PubMed] [Google Scholar]
  39. Cassard-Doulcier A-M, Perlemuter G. Inflammation hépatique liée à l’obésité (NASH). Oléagineux Corps gras Lipides 2011 ; 18 : 21–26. [CrossRef] [Google Scholar]
  40. L’Hermitte A, Pham S, Cadoux M, Couty J-P Hépatopathies stéatosiques non alcooliques. Med/Sci (Paris) 2016 ; 32 : 1023–1026. [Google Scholar]
  41. Yang L, Jhaveri R, Huang J, et al. Endoplasmic reticulum stress, hepatocyte CD1d and NKT cell abnormalities in murine fatty livers. Lab Invest 2007 ; 87 : 927–937. [CrossRef] [PubMed] [Google Scholar]
  42. Szpigel A, Hainault I, Carlier A, et al. Lipid environment induces ER stress, TXNIP expression and inflammation in immune cells of individuals with type 2 diabetes. Diabetologia 2018 ; 61 : 399–412. [CrossRef] [PubMed] [Google Scholar]
  43. Deniaud A, Sharaf el dein O, Maillier E, et al. Endoplasmic reticulum stress induces calcium-dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosis. Oncogene 2008 ; 27 : 285–299. [Google Scholar]
  44. Gonzalez-Rodriguez A, Mayoral R, Agra N, et al. Impaired autophagic flux is associated with increased endoplasmic reticulum stress during the development of NAFLD. Cell Death Dis 2014 ; 5 : e1179. [CrossRef] [PubMed] [Google Scholar]
  45. Bailly-Maitre B, Belgardt BF, Jordan SD, et al. Hepatic Bax inhibitor-1 inhibits IRE1alpha and protects from obesity-associated insulin resistance and glucose intolerance. J Biol Chem 2010 ; 285 : 6198–6207. [CrossRef] [PubMed] [Google Scholar]
  46. Bailly-Maitre B, Fondevila C, Kaldas F, et al. Cytoprotective gene bi-1 is required for intrinsic protection from endoplasmic reticulum stress and ischemia-reperfusion injury. Proc Natl Acad Sci USA 2006 ; 103 : 2809–2814. [CrossRef] [Google Scholar]
  47. Schattenberg JM, Singh R, Wang Y, et al. JNK1 but not JNK2 promotes the development of steatohepatitis in mice. Hepatology 2006 ; 43 : 163–172. [CrossRef] [PubMed] [Google Scholar]
  48. Yamaguchi K, Yang L, McCall S, et al. Inhibiting triglyceride synthesis improves hepatic steatosis but exacerbates liver damage and fibrosis in obese mice with nonalcoholic steatohepatitis. Hepatology 2007 ; 45 : 1366–1374. [CrossRef] [PubMed] [Google Scholar]
  49. Wang D, Wei Y, Pagliassotti MJ. Saturated fatty acids promote endoplasmic reticulum stress and liver injury in rats with hepatic steatosis. Endocrinology 2006 ; 147 : 943–951. [CrossRef] [PubMed] [Google Scholar]
  50. Hetz C, Bernasconi P, Fisher J, et al. Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha. Science 2006 ; 312 : 572–576. [Google Scholar]
  51. Rieusset J. Endoplasmic reticulum-mitochondria calcium signaling in hepatic metabolic diseases. Biochim Biophys Acta Mol Cell Res 2017 ; 1864 : 865–876. [CrossRef] [PubMed] [Google Scholar]
  52. Xu C, Xu W, Palmer AE, Reed JC. BI-1 regulates endoplasmic reticulum Ca2+ homeostasis downstream of Bcl-2 family proteins. J Biol Chem 2008 ; 283 : 11477–11484. [CrossRef] [PubMed] [Google Scholar]
  53. Taouji S, Chevet E. Modulation pharmacologique de la réponse au stress du réticulum endoplasmique : potentiel thérapeutique en cancérologie. Med Sci (Paris) 2015 ; 31 : 667–673. [CrossRef] [EDP Sciences] [PubMed] [Google Scholar]

Current usage metrics show cumulative count of Article Views (full-text article views including HTML views, PDF and ePub downloads, according to the available data) and Abstracts Views on Vision4Press platform.

Data correspond to usage on the plateform after 2015. The current usage metrics is available 48-96 hours after online publication and is updated daily on week days.

Initial download of the metrics may take a while.