Advances in cell death - related signaling pathways in acute-on-chronic liver failure

Huang, Liqiao; Liu, Jie; Bie, Caiqun; Liu, Helu; Ji, Yichun; Chen, Dongfeng; Zhu, Meiling; Kuang, Weihong

doi:10.1016/j.clinre.2021.101783

Cited by 8 publications

(5 citation statements)

References 50 publications

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“…Redox imbalance in macromolecular biosynthesis leads to liver diseases which can be inflammatory, non-inflammatory, and degenerative, all with the possibility of liver fibrosis progression [ 1 ]. Chronic liver damage caused by mycotoxins induces redox-homeostatic up-regulation in liver cells and interrupts liver function and hepatocyte stimulation that activates apoptotic signaling [ 2 ]. The synthesis of different mycotoxins genera is carried out by sequential oxidative, alkylating, or condensing enzymatic reactions in the metabolism of malonate, mevalonate, acetate, or amino acids [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

The Azadirachta indica (Neem) Seed Oil Reduced Chronic Redox-Homeostasis Imbalance in a Mice Experimental Model on Ochratoxine A-Induced Hepatotoxicity

Nikolova

Ananiev²,

Иванов³

et al. 2022

Antioxidants

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Liver damage severity depends on both the dose and the exposure duration. Oxidative stress may increase the Ochratoxine-A (OTA) hepatotoxicity and many antioxidants may counteract toxic liver function. The present study aims to investigate the hepatoprotective potential of Azadirachta indica A (A.indica; neem oil) seed oil to reduce acute oxidative disorders and residual OTA toxicity in a 28-day experimental model. The activity of antioxidant and hepatic enzymes, cytokines and the levels of oxidative stress biomarkers –MDA, GSPx, Hydroxiproline, GST, PCC, AGEs, PGC-1, and STIR-1 were analyzed by ELISA. The free radicals ROS and RNS levels were measured by EPR. The protective effects were studied in BALB/C mice treated with A. indica seed oil (170 mg/kg), alone and in combination with OTA (1.25 mg/kg), by gavage daily for 28 days. At the end of the experiment, mice treated with OTA showed changes in liver and antioxidant enzymes, and oxidative stress parameters in the liver and blood. A.indica oil significantly reduced oxidative stress and lipid peroxidation compared to the OTA group. In addition, the hepatic histological evaluation showed significant adipose tissue accumulation in OTA-treated tissues, while treatment with 170 mg/kg A.indica oil showed moderate adipose tissue accumulation.

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Section: Introductionmentioning

confidence: 99%

The Azadirachta indica (Neem) Seed Oil Reduced Chronic Redox-Homeostasis Imbalance in a Mice Experimental Model on Ochratoxine A-Induced Hepatotoxicity

Nikolova

Ananiev²,

Иванов³

et al. 2022

Antioxidants

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“…The results also showed MHLQD significantly suppressed cleaved-caspase-3 and p-MLKL expression, compared with the ACLF and the ALF group ( Figure 3 B,D). Hepatocyte death induced by inflammatory cells-released inflammatory mediators is the direct cause of liver destruction [ 23 , 24 ]. Both apoptosis and necroptosis have been reported to be induced during ALF and ACLF [ 25 , 26 ].…”

Section: Resultsmentioning

confidence: 99%

Ancient Herbal Formula Mahuang Lianqiao Chixiaodou Decoction Protects Acute and Acute-on-Chronic Liver Failure via Inhibiting von Willebrand Factor Signaling

Lin

Ling

Yan

et al. 2022

Cells

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Background: Acute liver failure (ALF) and acute-on-chronic liver failure (ACLF) are characterized by systemic inflammation and high mortality, but there is no effective clinical treatment. As a classic traditional Chinese medicine (TCM) formula, MaHuang-LianQiao-ChiXiaoDou decoction (MHLQD) has been used clinically for centuries to treat liver diseases. Methods: The LPS/D−GalN-induced ALF mice model and the CCl4+LPS/D−GalN-induced ACLF mice model were used to observe the therapeutic effects of MHLQD on mice mortality, hepatocytes death, liver injury, and immune responses. Results: MHLQD treatment significantly improved mice mortality. Liver injury and systemic and hepatic immune responses were also ameliorated after MHLQD treatment. Mechanistically, proteomic changes in MHLQD-treated liver tissues were analyzed and the result showed that the thrombogenic von Willebrand factor (VWF) was significantly inhibited in MHLQD-treated ALF and ACLF models. Histological staining and western blotting confirmed that VWF/RAP1B/ITGB3 signaling was suppressed in MHLQD-treated ALF and ACLF models. Furthermore, mice treated with the VWF inhibitor ADAMTS13 showed a reduced therapeutic effect from MHLQD treatment. Conclusions: Our study indicated that MHLQD is an effective herbal formula for the treatment of ALF and ACLF, which might be attributed to the protection of hepatocytes from death via VWF/RAP1B/ITGB3 signaling.

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“…Damage-associated molecular patterns are immunogenic molecules released by dying or dead cells that contribute to inflammation and other aspects of ACLF pathophysiology. While some authors postulate that apoptosis is the predominant mode of cell death during ACLF [73,74], evidence supports a major contribution of non-apoptotic pathways, including necroptosis and pyroptosis [75,76].…”

Section: Aclf and Cell Deathmentioning

confidence: 99%

“…Moreover, Khanam et al [78] showed that necrosis can be prevented by inhibiting the inflammatory process triggered by the CXCR1/2 receptors, which are highly expressed in peripheral blood mononuclear cells from ACLF patients. Even though pyroptosis has not been addressed in the context of ACLF, there is little evidence of the activation of this cell death pathway in acute liver failure (ALF) [76]. Li et al [79] described that pyroptosis contributes to macrophage recruitment and inflammatory signaling in an ALF model of LPS + GalN.…”

Section: Aclf and Cell Deathmentioning

confidence: 99%

Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression

Osna,

Tikhanovich,

Ortega-Ribera

et al. 2024

Biomolecules

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Alcohol-associated liver disease (ALD) is a substantial cause of morbidity and mortality worldwide and represents a spectrum of liver injury beginning with hepatic steatosis (fatty liver) progressing to inflammation and culminating in cirrhosis. Multiple factors contribute to ALD progression and disease severity. Here, we overview several crucial mechanisms related to ALD end-stage outcome development, such as epigenetic changes, cell death, hemolysis, hepatic stellate cells activation, and hepatic fatty acid binding protein 4. Additionally, in this review, we also present two clinically relevant models using human precision-cut liver slices and hepatic organoids to examine ALD pathogenesis and progression.

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Advances in cell death - related signaling pathways in acute-on-chronic liver failure

Cited by 8 publications

References 50 publications

The Azadirachta indica (Neem) Seed Oil Reduced Chronic Redox-Homeostasis Imbalance in a Mice Experimental Model on Ochratoxine A-Induced Hepatotoxicity

The Azadirachta indica (Neem) Seed Oil Reduced Chronic Redox-Homeostasis Imbalance in a Mice Experimental Model on Ochratoxine A-Induced Hepatotoxicity

Ancient Herbal Formula Mahuang Lianqiao Chixiaodou Decoction Protects Acute and Acute-on-Chronic Liver Failure via Inhibiting von Willebrand Factor Signaling

Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression

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