scholarly journals Heparan sulfate promotes recovery from acute liver injury: Inhibition of progressive cell death or enhanced regeneration?

Hepatology ◽  
2017 ◽  
Vol 66 (5) ◽  
pp. 1381-1383 ◽  
Author(s):  
Udayan Apte ◽  
Neil Kaplowitz
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Heparan Sulfate ◽  
Acute Liver Injury

scholarly journals Liver Autophagy in Anorexia Nervosa and Acute Liver Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Marouane Kheloufi ◽  
Chantal M. Boulanger ◽  
François Durand ◽  
Pierre-Emmanuel Rautou
Keyword(s):  
Cell Death ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism ◽  
Liver Insufficiency ◽  
Electron Microscopy Analysis ◽  
Microscopy Analysis ◽  
Rescue Mechanism ◽  
Liver Cell Death

Autophagy, a lysosomal catabolic pathway for long-lived proteins and damaged organelles, is crucial for cell homeostasis, and survival under stressful conditions. During starvation, autophagy is induced in numerous organisms ranging from yeast to mammals, and promotes survival by supplying nutrients and energy. In the early neonatal period, when transplacental nutrients supply is interrupted, starvation-induced autophagy is crucial for neonates’ survival. In adult animals, autophagy provides amino acids and participates in glucose metabolism following starvation. In patients with anorexia nervosa, autophagy appears initially protective, allowing cells to copes with nutrient deprivation. However, when starvation is critically prolonged and when body mass index reaches 13 kg/m2or lower, acute liver insufficiency occurs with features of autophagic cell death, which can be observed by electron microscopy analysis of liver biopsy samples. In acetaminophen overdose, a classic cause of severe liver injury, autophagy is induced as a protective mechanism. Pharmacological enhancement of autophagy protects against acetaminophen-induced necrosis. Autophagy is also activated as a rescue mechanism in response to Efavirenz-induced mitochondrial dysfunction. However, Efavirenz overdose blocks autophagy leading to liver cell death. In conclusion, in acute liver injury, autophagy appears as a protective mechanism that can be however blocked or overwhelmed.

miR-223 represents a biomarker in acute and chronic liver injury

2017 ◽  
Vol 131 (15) ◽  
pp. 1971-1987 ◽  
Author(s):  
Florian Schueller ◽  
Sanchari Roy ◽  
Sven Heiko Loosen ◽  
Jan Alder ◽  
Christiane Koppe ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Liver Diseases ◽  
Acute Liver Injury ◽  
Chronic Liver ◽  
Published Data ◽  
Duct Ligation

Background: Dysregulation of miRNAs has been described in tissue and serum from patients with acute and chronic liver diseases. However, only little information on the role of miR-223 in the pathophysiology of acute liver failure (ALF) and liver cirrhosis is available. Methods: We analysed cell and tissue specific expression levels as well as serum concentrations of miR-223 in mouse models of acute (hepatic ischaemia and reperfusion, single CCl4 injection) and chronic (repetitive CCl4 injection, bile duct ligation (BDL)) liver diseases. Results were validated in patients and correlated with clinical data. The specific hepatic role of miR-223 was analysed by using miR-223−/− mice in these models. Results: miR-223 expression was significantly dysregulated in livers from mice after induction of acute liver injury and liver fibrosis as well as in liver samples from patients with ALF or liver cirrhosis. In acute and chronic models, hepatic miR-223 up-regulation was restricted to hepatocytes and correlated with degree of liver injury and hepatic cell death. Moreover, elevated miR-223 expression was reflected by significantly higher serum levels of miR-223 during acute liver injury. However, functional in vitro and in vivo experiments revealed no differences in the degree of liver cell death and liver fibrosis as miR-223−/− mice behaved identical with wild-type (wt) mice in all tested models. Conclusion: miR-223 represents a promising diagnostic marker in a panel of serum markers of liver injury. Together with previously published data, our results highlight that the role of miR-223 in the pathophysiology of the liver is complex and needs further analysis.

scholarly journals The protein tyrosine kinase SYK regulates the alternative p38 activation in liver during acute liver inflammation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Bo-Ram Bang ◽  
Kyung Ho Han ◽  
Goo-Young Seo ◽  
Michael Croft ◽  
Young Jun Kang
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Host Defense ◽  
Protein Tyrosine Kinase ◽  
Inflammatory Responses ◽  
Acute Liver Injury ◽  
Critical Role ◽  
Liver Inflammation ◽  
Hepatocyte Death

AbstractTwo distinct p38 signaling pathways, classical and alternative, have been identified to regulate inflammatory responses in host defense and disease development. The role of alternative p38 activation in liver inflammation is elusive, while classical p38 signaling in hepatocytes plays a role in regulating the induction of cell death in autoimmune-mediated acute liver injury. In this study, we found that a mutation of alternative p38 in mice augmented the severity of acute liver inflammation. Moreover, TNF-induced hepatocyte death was augmented by a mutation of alternative p38, suggesting that alternative p38 signaling in hepatocytes contributed more significantly to the pathology of acute liver injury. Furthermore, SYK-Vav-1 signaling regulates alternative p38 activation and the downregulation of cell death in hepatocytes. Therefore, it is suggested that alternative p38 signaling in the liver plays a critical role in the induction and subsequent pathological changes of acute liver injury. Collectively, our results imply that p38 signaling in hepatocytes plays a crucial role to prevent excessive liver injury by regulating the induction of cell death and inflammation.

scholarly journals Paramylon from Euglena gracilis Prevents Lipopolysaccharide-Induced Acute Liver Injury

2022 ◽  
Vol 12 ◽  
Author(s):  
Yunhao Xie ◽  
Jin Li ◽  
Huan Qin ◽  
Qing Wang ◽  
Zixi Chen ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Euglena Gracilis ◽  
Target Genes ◽  
Acute Liver Injury ◽  
Biological Effects ◽  
Nutritional Supplement ◽  
M2 Macrophage ◽  
Molecular Weights ◽  
Life Threatening

Acute liver injury (ALI) is a life-threatening syndrome with high mortality and lacks effective therapies. Rodents under LPS (lipopolysaccharide)/D-Gal (D-galactosamine) stress mimic ALI by presenting dramatically increased inflammation and cell death in the liver. Euglena gracilis, functioning like dietary fiber, is commonly used as a paramylon (Pa)-rich nutritional supplement that has various biological effects such as regulating immune system, anti-obesity, and anti-tumor. Here, we found that Pa or sonicated and alkalized paramylon (SA-Pa) alleviated the LPS/D-Gal-induced hepatic histopathological abnormalities in mice. Compared with Pa, SA-Pa had lower molecular weights/sizes and showed better efficacy in alleviating injury-induced hepatic functions, as well as the transcriptional levels of inflammatory cytokines. Moreover, SA-Pa treatment promoted M2 macrophage activation that enhanced the anti-inflammatory function in the liver, and downregulated STAT3 target genes, such as Fos, Jun, and Socs3 upon the injury. Meanwhile, SA-Pa treatment also alleviated apoptosis and necroptosis caused by the injury. Our results demonstrated that SA-Pa efficiently protected the liver from LPS/D-Gal-induced ALI by alleviating inflammation and cell death.

scholarly journals Deficiency of miR‐208a Exacerbates CCl 4 ‐Induced Acute Liver Injury in Mice by Activating Cell Death Pathways

2020 ◽  
Vol 4 (10) ◽  
pp. 1487-1501
Author(s):  
Shashi Bala ◽  
Charles D. Calenda ◽  
Donna Catalano ◽  
Mrigya Babuta ◽  
Karen Kodys ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Cell Death Pathways

Down-regulation of miR-192-5p protects from oxidative stress-induced acute liver injury

2016 ◽  
Vol 130 (14) ◽  
pp. 1197-1207 ◽  
Author(s):  
Sanchari Roy ◽  
Fabian Benz ◽  
Jan Alder ◽  
Heike Bantel ◽  
Joern Janssen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Liver Injury ◽  
Therapeutic Approach ◽  
Acute Liver Injury ◽  
Down Regulation

In the present study, we demonstrate that miR-192-5p is critically involved in the regulation of cell death during acute liver injury, highlighting a potential miR-based therapeutic approach in this setting.

Circulating apoptotic and necrotic cell death markers in patients with acute liver injury

2011 ◽  
Vol 31 (8) ◽  
pp. 1127-1136 ◽  
Author(s):  
Darren G. N. Craig ◽  
Patricia Lee ◽  
Elizabeth A. Pryde ◽  
Gail S. Masterton ◽  
Peter C. Hayes ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Necrotic Cell Death ◽  
Necrotic Cell
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