Does Acetaminophen Affect The Liver – Literature Review: Weiskirchen, R.; Friedman, S.L. Hepatic stellate cells: methods and protocols, 1st ed.; Weiskirchen, R., Friedman, S.L., Eds.; Methods in Molecular Biology 2669; Humana Press: New York, NY, USA, 2023; ISBN 978-1-07-163206-2; ISBN: 978-1-0716-3207-9
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Does Acetaminophen Affect The Liver
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Myeloid Dj 1 Deficiency Protects Acetaminophen Induced Acute Liver Injury Through Decreasing Inflammatory Response
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By Bharat Bhushan Bharat Bhushan Skillit Preprints.org Google Scholar 1, 2, * and Udayan Apte Udayan Apte Skillit Preprints.org Google Scholar 3
Interruption Of Bile Acid Uptake By Liver Cells After Paracetamol Overdose Mitigates Liver Damage
Pittsburgh Liver Research Center, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
Received: 28 March 2023 / Revised: 16 May 2023 / Approved: 25 May 2023 / Published: 9 June 2023
Liver regeneration is a response to injury and tissue damage. It is known that liver regeneration plays an important role in recovery following acetaminophen (APAP)-induced hepatotoxicity, which is the leading cause of acute liver failure (ALF) in the US. Regeneration increases in proportion to the degree of liver injury upon increasing APAP, ultimately leading to re-injury and spontaneous recovery in most cases. However, high levels of APAP lead to liver damage and liver failure, resulting in poor recovery and death. Intercellular communication between different cells in the liver is essential for an efficient response following APAP hepatotoxicity. Various non-parenchymal cells such as macrophages, stellate cells, and endothelial cells produce mediators that are essential for hepatocyte proliferation. Liver regeneration is controlled by the coordinated action of several reproductive signaling pathways, including multiple kinases, nuclear receptors, transcription factors, transcription factors, which are regulated by cytokines, growth factors, and endobiotics. The appearance of anti-proliferative signaling pathways causes cell arrest and impaired liver regeneration after increased APAP. may be important in the development of future treatments for APAP-induced ALF.
The liver has an amazing ability to regenerate after surgery, disease, and liver injury or medication. The liver is the only organ that recovers its original weight even after two-thirds of the muscle mass [1]. All types of cells in the liver, including hepatocytes, cholangiocytes, hepatic stellate cells, and endothelial cells, often proliferate to replace their own cells and eventually achieve the original liver damage and function. The phenomenon that controls the growth of the liver in normal conditions and especially during regeneration is called hepatostat [1, 2]. Liver regeneration is controlled by the coordinated actions of several signaling pathways, including many kinases, nuclear receptors, transcription factors, transcription factors, which are regulated by cytokines, growth factors, antibiotics such as bile acids and hormones [3]. The adaptive responses of a healthy liver are very strong, and the removal of any signaling pathway usually has little effect due to the limited number of signaling pathways [1].
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Many studies have shown that liver regeneration plays an important role in recovery after acetaminophen (APAP) overdose, which is a serious medical problem [4, 5, 6, 7, 8, 9]. APAP is one of the most widely used over-the-counter analgesics and is considered to be the safest drug in the world. However, increased APAP leads to severe liver injury that includes hepatocyte cell death and centrilobular necrosis, leading to acute liver failure (ALF) in severe cases. APAP overdose is the leading cause of ALF in the United States and the Western world [10]. APAP-induced hepatocyte death and centrilobular necrosis is triggered by the toxic metabolite NAPQI (N-acetyl-p-benzoquinone imine), which is usually released after conjugation with cellular glutathione (GSH). The increased NAPQI caused by APAP reduces GSH stores and produces cell proteins (mainly mitochondrial proteins), which eventually lead to mitochondrial damage, the release of mediators of cell death of mitochondria, and necrosis [11, 12]. Interestingly, most APAP patients recover spontaneously due to the high rate of reperfusion. During this regeneration, the dead hepatocytes are replaced by newly formed cells, from the normal hepatocytes surrounding the necrotic zone that restore the liver mass and function. However, in severe cases, spontaneous recovery does not occur because the delay and inhibition of liver regeneration lead to death. Several studies have associated a stronger liver response with better outcomes in ALF patients treated with APAP [13, 14]. Therefore, timely stimulation of liver regeneration is a therapeutic strategy for APAP-induced ALF, and understanding the mechanisms of liver regeneration is important to develop possible therapeutic targets. Medical treatment can be very beneficial because liver damage is already established in many patients by the time they go to the hospital and is difficult to control. This is evident from the fact that N-acetyl cysteine ​​​​​​​​(NAC), the only medical treatment for APAP-induced ALF, based on the early intervention of liver injury, does not work in late patients [15]. Conversely, recovery methods can be used later.
In the past, most research to understand how the liver regenerates has focused on the type of partial hepatectomy, which involves the regeneration of a healthy liver [16]. However, APAP hepatotoxicity is complicated by extensive cell death and persistent inflammation. These mechanisms and associated signaling mediators complexly regulate the hepatic response after APAP hepatotoxicity. A recent study has shown that the response and the mechanisms that support the regeneration of the liver are very different in this dangerous environment compared to a healthy liver [17]. Additionally, other medical conditions such as alcoholic or non-alcoholic fatty liver disease can also affect the liver’s response. Liver regeneration after hepatectomy in healthy livers is very similar compared to regeneration in response to APAP hepatotoxicity, where many injury-related factors inhibit proliferation [17]. Therefore, in recent years, research has focused mainly on explaining the mechanisms of liver damage in APAP-induced liver injury models. Methods to specifically promote or inhibit liver regeneration after APAP hepatotoxicity, their dose-response characteristics, and the role of different liver cells in liver regeneration are discussed in this review. In addition, factors to consider when designing studies to investigate liver regeneration following APAP hepatotoxicity are also discussed.
Hepatocyte proliferation and liver regeneration occur as a secondary response to exposure to toxic chemicals [18]. These include toxic substances that harm different areas of the liver, including centrilobular hepatotoxicants (such as carbon tetrachloride, thioacetamide, and APAP) and periportal hepatotoxicants (such as allyl alcohol) [9, 18, 19, 20, 21]. Characteristics related to the degree of liver regeneration following acute liver damage have been extensively studied and reviewed previously [18]. These studies have confirmed that the regeneration of the liver increases in proportion to the injury of the liver by increasing the dose of the poison [18, 20]. There is also a gradual delay in the liver’s response to increasing doses. However, the increase in the increase in the regeneration of the liver eliminates the delay in the response to the regeneration of a certain level, ultimately causing the damage to be destroyed and recovered. Therefore, to a certain extent, the stimulation of the regeneration of the liver occurs according to the injury. Beyond this dose, liver regeneration is greatly reduced and delayed with increasing doses. This leads to uncontrolled progression of liver injury leading to failure of recovery and death [9, 18]. For example, the relationship with this dose of liver regeneration has been well demonstrated for thioacetamide using different doses (50, 150, 300 and 600 mg/kg) during 0-96 h in rats. Liver changes, up to 300 mg/kg dose of thioacetamide increased the rate of liver injury leading to complete recovery. However, at a dose of 600 mg/kg liver regeneration is severely disrupted and delays lead to high mortality [20]. In addition, if proliferation is inhibited by anti-mitotic agents (such as colchicine) after toxic doses that usually cause liver regeneration and sudden recovery, it also leads to the development of injury and failure to recover [18, 22]. These studies also emphasize the importance of liver regeneration for recovery as well
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