[1] Zaccherini G, Aguilar F, Caraceni P, et al. Assessing the role of amino acids in systemic inflammation and organ failure in patients with ACLF. J Hepatol,2021,74:11 17-1131.
[2] Moreau R, Clària J, Aguilar F, et al. CANONIC study investigators of the EASL clif consortium; European foundation for the study of chronic liver failure (EF clif). Blood metabolomics uncovers inflammation-associated mitochondrial dysfunction as a potential mechanism underlying ACLF. J Hepatol,2020,72:688-701.
[3] Clària J, Moreau R, Fenaille F, et al. CANONIC study investigators of the EASL clif consortium, grifols chair and the European foundation for the study of chronic liver failure (EF clif). Orchestration of tryptophan-kynurenine pathway, acute decompensation, and acute-on-chronic liver failure in cirrhosis. Hepatology, 2019,69:1686-1701.
[4] Korf H, Du Plessis J, Van Pelt J, et al.Inhibition of glutamine synthetase in monocytes from patients with acute-on-chronic liver failure resuscitates their antibacterial and inflammatory capacity. Gut,2019,68:1872-1883.
[5] Brealey D, Brand M, Hargreaves I, et al.Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet,2002,360:219-223.
[6] Takahashi W, Watanabe E, Fujimura L, et al. Kinetics and protective role of autophagy in a mouse cecal ligation and puncture-induced sepsis. Crit Care, 2013,17:R160.
[7] Tardif N, Polia F, Tj?der I, et al. Autophagy flux in critical illness, a translational approach. Sci Rep,2019,9:10762.
[8] Ebadi M, Bhanji RA, Mazurak VC, et al. Sarcopenia in cirrhosis: from pathogenesis to interventions. J Gastroenterol,2019,54:845-859.
[9] Schefold JC, Wollersheim T, Grunow JJ, et al. Muscular weakness and muscle wasting in the critically ill. J Cachexia Sarcopenia Muscle,2020,11:1399-1412.
[10] Schefold JC, Bierbrauer J, Weber-Carstens S. Intensive care unit-acquired weakness (ICUAW) and muscle wasting in critically ill patients with severe sepsis and septic shock. J Cachexia Sarcopenia Muscle,2010,1:147-157.
[11] Praktiknjo M, Book M, Luetkens J,et al. Fat-free muscle mass in magnetic resonance imaging predicts acute-on-chronic liver failure and survival in decompensated cirrhosis. Hepatology,2018,67:1014-1026.
[12] Zimmers TA, Davies MV, Koniaris LG, et al. Induction of cachexia in mice by systemically administered myostatin. Science,2002,296:1486-1488.
[13] McFarlane C, Plummer E, Thomas M,et al. Myostatin induces cachexia by activating the ubiquitin proteolytic system through an NF-kappaB-independent, FoxO1-dependent mechanism. J Cell Physiol,2006,209:501-514.
[14] Davuluri G, Krokowski D, Guan BJ, et al. Metabolic adaptation of skeletal muscle to hyperammonemia drives the beneficial effects of l-leucine in cirrhosis. J Hepatol, 2016,65:929-937.
[15] Dasarathy S, McCullough AJ, Muc S, et al. Sarcopenia associated with portosystemic shunting is reversed by follistatin. J Hepatol 201 1;54:915-921.
[16] Qiu J, Thapaliya S, Runkana A, et al. Hyperammonemia in cirrhosis induces transcriptional regulation of myostatin by an NF-jB-mediated mechanism. Proc Natl Acad Sci USA,2013,10:18162-18167.
[17] Kumar A, Davuluri G, Silva RNE,et al. Ammonia lowering reverses sarcopenia of cirrhosis by restoring skeletal muscle proteostasis. Hepatology,2017,65:2045-2058.
[18] Goossens C, Weckx R, Derde S, et al. Adipose tissue protects against sepsis-induced muscle weakness in mice: from lipolysis to ketones. Crit Care, 2019,23:236.
[19] Langley RJ, Tsalik EL, van Velkinburgh JC, et al. An integrated clinico-metabolomic model improves prediction of death in sepsis. Sci Transl Med, 2013,5:195ra95.
[20] Revell V, Mann A, Mäntele S, et al. Identification of human plasma metabolites exhibiting time-of-day variation using an untargeted liquid chromatography-mass spectrometry metabolomic approach. Chronobiol Int,2012,29:868-881.
[21] Coenraad MJ, Artru F. Amino acids in acute-on-chronic liver failure: Another piece of the puzzle? J Hepatol,2021,74:1015-1017. |
