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Fetal Growth Factors*
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
Philip A. Gruppuso, Thomas R. Curran, Roderick I. Bahner
Much of our current knowledge of the regulation of liver growth can be traced to in vivo studies on liver regeneration following partial hepatectomy in the rat. Partial hepatectomy leads to an initial alteration in hepatocytes from a quiescent to an actively replicating phenotype, resulting in restoration of liver mass.5,6 This is followed by differentiation and restoration of normal architecture and function. The events following partial hepatectomy have been used to identify growth factors and proto-oncogenes involved in regulation of liver growth, such as the transforming growth factors, TGF-α7 and TGF-β.8 Possible parallels between liver regeneration and fetal hepatic growth have influenced our recent studies (e.g., those on the ontogeny of TGF receptors).9
Biological Perspectives of Cytokine and Hormone Networks
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Aleksander Koj, Jack Gauldie, Heinz Baumann
Liver regeneration is a highly complex process triggered by hepatocyte growth factors (HGFs) which also appear to be potent mitogens for some epidermal and epithelial cells, but which inhibit proliferation of hepatomas (for references, see References 100 and 101). We observed that human recombinant HGF stimulates the synthesis of α2-macroglobulin in primary cultures of rat hepatocytes.102 Its effects on the synthesis of AP proteins are broader in Hep G2 cells, where HGF inhibits the synthesis of albumin, but increases the basal production of fibrinogen, α1-antichymotrypsin, and α1-proteinase inhibitor (Figure 3). However, in cells stimulated by high concentrations of IL-6, HGF decreases the maximum response of haptoglobin, fibrinogen, and α1-antichymotrypsin. A similar phenomenon was observed with insulin (Figure 3). On the other hand, TGFβ increased the production of α1 antichymotrypsin and al-proteinase inhibitor in Hep G2 cells, even at high concentrations of IL-6. These results emphasize again the existence of intricate networks of cytokines and cellular growth factors in the regulation of the liver AP response.
Auxiliary Heterotopic Rat Liver Transplantation
Published in Waldemar L. Olszewski, CRC Handbook of Microsurgery, 2019
Our observations and concept of liver regeneration do not support the opinions of other researchers on this matter: they propose the existence of a so-called specific hepatotrophic portal factor that initiates and controls liver regeneration.26–29 The supposed site of production of this factor in the splanchnic organ is not clear, neither is its composition.26,30–33
Flavonoid constituents and protective efficacy of Citrus reticulate (Blanco) leaves ethanolic extract on thioacetamide-induced liver injury rats
Published in Biomarkers, 2023
Usama W. Hawas, Mohamed A. El-Ansari, Abeer F. Osman, Asmaa F. Galal, Lamia T. Abou El-Kassem
The liver is a critical organ in the human body that is responsible for the regulation of several metabolic functions and physiological processes. Its ability to detoxify xenobiotics makes it especially crucial for maintaining bodily health. Several mechanisms have been proposed to explain the hepatotoxicity of viral or non-viral hepatitis. In both cases, the cornerstone mechanisms are inflammation and oxidative stress-induced membrane lipid peroxidation (Tarocchi et al.2014). In addition, the liver’s self-healing and regenerative capacity can lead to excessive accumulation of extracellular matrix (ECM) proteins such as collagen, followed by progressive tissue scarring, cirrhosis, and loss of liver function. Despite advancements in contemporary medicine, there is no effective treatment strategy for enhancing liver regeneration, protecting the liver, or stimulating hepatic function (Madrigal-Santillán et al. 2014). Current drugs, such as pegylated interferon-alpha (IFN-α) and ribavirin, used to treat hepatitis virus infection, are not always successful in curing patients, and some of them may not tolerate this treatment. Similar restrictions have been found with silymarin, the most well-known hepatoprotective compound, when used to treat chronic liver damage such as cirrhosis. Thus, it is necessary to identify highly effective drugs for the treatment of liver diseases, emphasising their low toxicity.
Corosolic acid inhibits tumour growth without compromising associating liver partition and portal vein ligation-induced liver regeneration in rats
Published in Annals of Medicine, 2022
Jinwei Zhao, Weiyi Zhao, Hongyue Xu, Wenjing Luan, Xuefei Wang, Yimu Fang, Lu Yu
In patients with liver tumours, liver regeneration may induce the growth of occult lesions. There is an urgent need for drugs that can inhibit tumour growth without compromising liver regeneration. Chloroquine, an autophagy inhibitor, has been used to inhibit tumour growth; however, because it compromises liver regeneration, it cannot be used for hepatectomy, split-liver transplantation, or living-donor liver transplantation in patients with tumours [31]. Accruing studies have shown that CA displays anticancer activity in various types of in vitro and in vivo tumours [16,17]. Our results indicate that, at a dosage of 20 mg/kg every other day for 12 days, the administration of CA may have suppressed tumour-cell proliferation and tumour growth without compromising ALPPS-induced liver regeneration. In addition, although the surgical ALPPS procedure appeared to have caused an inflammatory response in the lungs, kidneys, and liver (and even affected liver function), the administration of CA did not aggravate organ damage after ALPPS. Therefore, CA is an ideal potential drug for inhibiting the growth of occult lesions during ALPPS-induced liver regeneration. A drug typically used for treating obesity and type 2 diabetes, CA has shown excellent effects against diabetes in animal experiments and clinical trials [32]. Its anticancer activity in several types of tumours has recently attracted increasing attention from scholars. A growing number of studies have shown that CA suppresses tumour growth by modulating many cellular signalling pathways, including the STAT-3, NF-κB, and Wnt/β-catenin pathways.
HO-1 Protects Remnant Liver against Dysfunction after Major Hepatectomy in Humans
Published in Journal of Investigative Surgery, 2022
Ning He, Xiuni Sun, Zhenghui Hu, Feifan Wang, Yan Zhang, Xianwu Chen, Hongshen Wu, Xuejian Zhou, Shusen Zheng, Xiaodong Jin
After hepatectomy, LD is induced by many factors. The most important factor is liver regeneration, which can be reflected by liver capacity. Although other clinical factors such as liver cirrhosis, postoperative morbidity and changes in other treatments would affect postoperative liver regeneration, there is no strong correlation between the two [7]. According to preclinical studies, after liver resection, the proliferation of liver cells and the liver parenchymal remodeling are supported by renowned growth factors such as hepatocyte growth factor(HGF), and interleukin-6(IL)-6 and transforming growth factor (TGF)-β from hepatocytes and mesenchymal cells et al. [8] In our previous study, we demonstrated that restrain of HO-1 delayed liver proliferation, partly by downregulation of an HGF-Akt axis instead of IL-6 and TGF-β signaling in vivo and in vitro [5].