EDP Sciences logo
Authentification abonné
Rechercher
Menu
Accueil Tous les numéros Volume 36 / Numéro 2 (Février 2020) Med Sci (Paris), 36 2 (2020) 119-129 Références
Open Access
Numéro
Med Sci (Paris)
Volume 36, Numéro 2, Février 2020
Page(s) 119 - 129
Section M/S Revues
DOI https://doi.org/10.1051/medsci/2020008
Publié en ligne 4 mars 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] [PubMed] [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. [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. [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. [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]

Les statistiques affichées correspondent au cumul d'une part des vues des résumés de l'article et d'autre part des vues et téléchargements de l'article plein-texte (PDF, Full-HTML, ePub... selon les formats disponibles) sur la platefome Vision4Press.

Les statistiques sont disponibles avec un délai de 48 à 96 heures et sont mises à jour quotidiennement en semaine.

Le chargement des statistiques peut être long.