Reply to: "Lack of hepatic autophagy promotes severity of liver injury but not steatosis": ATG7 genetic variants behave as fatty liver disease progression modifiers
- PMID: 35985546
- DOI: 10.1016/j.jhep.2022.07.026
Reply to: "Lack of hepatic autophagy promotes severity of liver injury but not steatosis": ATG7 genetic variants behave as fatty liver disease progression modifiers
Conflict of interest statement
Conflict of interest The authors declare that they have no conflict of interest relevant to the present study. LV has received speaking fees from MSD, Gilead, AlfaSigma and AbbVie, served as a consultant for Gilead, Pfizer, AstraZeneca, Novo Nordisk, Intercept, Diatech Pharmacogenetics and Ionis Pharmaceuticals, and received research grants from Gilead. SR has served as a consultant for AstraZeneca, Celgene, Sanofi, Amgen, Akcea Therapeutics, Camp4, AMbys, Medacorp and Pfizer in the past 5 years, and received research grants from AstraZeneca, Sanofi and Amgen. Please refer to the accompanying ICMJE disclosure forms for further details.
Comment on
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Rare ATG7 genetic variants predispose patients to severe fatty liver disease.J Hepatol. 2022 Sep;77(3):596-606. doi: 10.1016/j.jhep.2022.03.031. Epub 2022 Apr 9. J Hepatol. 2022. PMID: 35405176
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Lack of hepatic autophagy promotes severity of liver injury but not steatosis.J Hepatol. 2022 Nov;77(5):1458-1459. doi: 10.1016/j.jhep.2022.05.015. Epub 2022 May 25. J Hepatol. 2022. PMID: 35643205 Free PMC article. No abstract available.