Liver Regeneration after Acetaminophen Hepatotoxicity

Bhushan, Bharat; Apte, Udayan

doi:10.1016/j.ajpath.2018.12.006

Cited by 130 publications

(148 citation statements)

References 64 publications

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“…The best-described models to study liver regeneration after acute damage are (1) liver resection (partial hepatectomy [3]) and (2) toxicological damage [6]. The essential difference is that the latter induces parenchymatic necrosis, and hepatocyte proliferation is integrated into a complex wound healing response with fibrosis and inflammation [6]. In contrast, 2/3 liver resection activates cell division in the absence of any cellular lesion [3].…”

Section: The Regulation Of the Cell Cycle Signaling And Metabolism mentioning

confidence: 99%

Cell cycle regulation in NAFLD: when imbalanced metabolism limits cell division

2020

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Cell division is essential for organismal growth and tissue homeostasis. It is exceptionally significant in tissues chronically exposed to intrinsic and external damage, like the liver. After decades of studying the regulation of cell cycle by extracellular signals, there are still gaps in our knowledge on how these two interact with metabolic pathways in vivo. Studying the cross-talk of these pathways has direct clinical implications as defects in cell division, signaling pathways, and metabolic homeostasis are frequently observed in liver diseases. In this review, we will focus on recent reports which describe various functions of cell cycle regulators in hepatic homeostasis. We will describe the interplay between the cell cycle and metabolism during liver regeneration after acute and chronic damage. We will focus our attention on non-alcoholic fatty liver disease, especially non-alcoholic steatohepatitis. The global incidence of non-alcoholic fatty liver disease is increasing exponentially. Therefore, understanding the interplay between cell cycle regulators and metabolism may lead to the discovery of novel therapeutic targets amenable to intervention.

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Section: The Regulation Of the Cell Cycle Signaling And Metabolism mentioning

confidence: 99%

Cell cycle regulation in NAFLD: when imbalanced metabolism limits cell division

2020

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“…2,27,28 They can proliferate induced by various stimulating factors to compensate liver volume and restore liver function. 3,29 With the in-depth study of the liver regeneration process, it is found that miRNAs are closely linked to liver regeneration. 30 In this study, we demonstrated that PMPs-derived miR-25-3p promoted proliferation of HHL-5 cells via targeting the BTG2 gene in vitro.…”

Section: Discussionmentioning

confidence: 99%

Platelet microparticles‐derived miR‐25‐3p promotes the hepatocyte proliferation and cell autophagy via reducing B‐cell translocation gene 2

et al. 2020

J of Cellular Biochemistry

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Platelets are critical regulators of liver regeneration, but the mechanisms are still not fully understood. Platelets have been shown to contain a wide variety of microRNAs (miRNAs) and play an important role in many diseases. However, the mechanism that how the platelet microparticles (PMPs)-derived miRNA regulate the hepatocyte proliferation is not very clear. In this study, we have successfully isolated and identified PMPs. We also found that PMPs, which could be well integrated into the HHL-5 cells, could upregulate the level of miR-25-3p in HHL-5 cells. Meanwhile, we found that PMPs-derived miR-25-3p promoted HHL-5 cells proliferation by accelerating cells into the S phase, and enhanced the autophagy by increasing the LC3II expression and reducing the P62 expression. Then, we proved that the miR-25-3p could target the B-cell translocation gene 2 (BTG2) and downregulate the expression levels of the BTG2 gene in HHL-5 cells. In addition, the overexpression of BTG2 significantly inhibited the proliferation and autophagy abilities of HHL-5 cells, while cotransfected miR-25-3p mimics or PMPs could partially rescue HHL-5 cells proliferation and autophagy. Furthermore, we proved that PMPs accelerated hepatocyte proliferation by regulating autophagy pathways. Therefore, PMPs-derived miR-25-3p promoted HHL-5 cell proliferation and autophagy by targeting BTG2, which may be a new therapeutic method for liver regeneration.

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“…Growth factors such as hepatocyte growth factor (HGF) are known to be crucial in liver regeneration, a continuous interest amongst researchers in their therapeutic application. However, higher concentrations of HGF in plasma were found in nonsurvivors as opposed to survivors, suggesting that interventions via other factors such as c-Met or TGF-β may be more effective for treatment [12]. In survivors, liver function is normally regained within three months.…”

Section: Figure 3: Acetaminophen Poisoning Treatment Optionsmentioning

confidence: 99%

Massive Acetaminophen Overdose

Stead

Jeong

Ganti

et al. 2020

Cureus

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The authors present a case of a fatal intentional acetaminophen (APAP) overdose and remind the physician how ubiquitous the drug is. This case presentation highlights the clinical presentation and treatment options for APAP overdose in unresponsive patients. In cases of massive APAP overdose (> 300 µg/ml plasma at four hours post-ingestion), prompt administration of N-acetylcysteine (NAC) and early hemodialysis are indicated.

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Liver Regeneration after Acetaminophen Hepatotoxicity

Cited by 130 publications

References 64 publications

Cell cycle regulation in NAFLD: when imbalanced metabolism limits cell division

Cell cycle regulation in NAFLD: when imbalanced metabolism limits cell division

Platelet microparticles‐derived miR‐25‐3p promotes the hepatocyte proliferation and cell autophagy via reducing B‐cell translocation gene 2

Massive Acetaminophen Overdose

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