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Liver Disease - Crossref

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Last Updated: 20 April 2022

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Clinical Progression of Metabolic-Associated Fatty Liver Disease Is Rare in a Danish Tertiary Liver Center

The evidence regarding non-invasive discrimination of simple steatohepatitis in metabolic-associated fatty liver disease and the danger of disease progression in patients with MAFLD is contradicting. Patients were divided by the presence of simple steatosis or steatohepatitis in liver biopsies. Patients with steatohepatitis had elevated BMIs, liver stiffness, HbA1c, and soluble, and were more likely to have metabolic syndrome at baseline than those with simple steatosis patients. According to the follow-up biopsy, twenty patients had the same fibrosis stage as the previous one, with seven advancing and four regressed.

Source link: https://doi.org/10.3390/jcm11092271


Chronic kidney disease after liver, cardiac, lung, heart–lung, and hematopoietic stem cell transplant

Chronic kidney disease is a major contributor to morbidity and mortality after transplantation. Although the immunosuppression regimen used for each of the transplant types, heart, liver, and HSCT are similar, patients with transplant complications may have different risk factors, such as CKD and CKD severity. Transplant physicians and nephrologists will have to collaborate to determine those patients at risk of developing CKD early to prevent its development and progression to end-stage renal disease early.

Source link: https://doi.org/10.1007/s00467-008-0785-2


Nonalcoholic Fatty Liver Disease: Pathogenesis and Therapeutics from a Mitochondria-Centric Perspective

A spectrum of conditions characterized by the accumulation of triglycerides in the liver is characterized by nonalcoholic fatty liver disease. This review will concentrate on the role of mitochondria in the pathophysiology of NAFLD and touch on some of the treatment options affecting mitochondria as well as metabolically important signaling pathways. Decreased ETC function, combined with increased rates of fatty acid beta-oxidation, leads to the accumulation of incomplete beta-oxidation products, which contribute to insulin resistance, as well as elevated levels of ROS.

Source link: https://doi.org/10.1155/2014/637027


Effect of modulation of PPAR-γ activity on Kupffer cells M1/M2 polarization in the development of non-alcoholic fatty liver disease

In vivo and in vitro, we investigated the relationship between PPAR- expression and macrophage polarization shifting since PPAR- has emerged as the master regulator of macrophage polarization. Here we showed that long-term high-fat diet improved Kupffer cells with M1-predominant phenotype and increased production of pro-inflammatory cytokines. Similarly, saturated fatty acids polarized Kupffer cells/macrophages to an M1-predominant phenotype, while n-3 PUFA polarized Kupffer cells/macrophages to an M2 phenotype, which was associated with the activation of the NF-B signal pathway and PPAR- respectively.

Source link: https://doi.org/10.1038/srep44612


B-cell lymphoma 6 alleviates nonalcoholic fatty liver disease in mice through suppression of fatty acid transporter CD36

Nonalcoholic fatty liver disease is a widespread disease that occurs in a variety of conditions, including steatohepatitis, advanced fibrosis, and liver cirrhosis. B-cell lymphoma 6 is a transcriptional antibody that is critical for germinal center B-cell cell differentiation, which is a transcriptional mediator. We induced hepatic BCL6 overexpression in our study using adeno-associated virus, as well as conditional liver-specific BCL6 knockout mice. In mice models maintained on a HFD diet, we discovered that BCL6 overexpression enhanced insulin resistance and hepatic steatosis. BCL6 is restraining CD36 transcription under physiological conditions. In a CD36-dependent manner, we show that the hepatocyte BCL6 blocks mouse NAFLD progression in mice, including deranged lipid accumulation and glucose metabolism. These findings indicate that BCL6 may potentially be targeted in NAFLD therapy.

Source link: https://doi.org/10.1038/s41419-022-04812-x


Therapeutic potential of macrophage colony-stimulating factor in chronic liver disease

We investigated the effect of CSF1-Fc on liver repair and fibrosis in C57BL/6J mice using a non-resolving toxin-induced model of chronic liver injury and fibrosis. In a model of partial hepatectomy in mice with established fibrosis, Acute CSF1-Fc treatment was also anti-fibrotic and pro-regenerative. These studies show that CSF1-dependent macrophages play both initiation and closure of fibrotic injury, as well as that CSF1-Fc has therapeutic potential in human liver disease.

Source link: https://doi.org/10.1242/dmm.049387


Telomerase reverse transcriptase acts in a feedback loop with NF-κB pathway to regulate macrophage polarization in alcoholic liver disease

A mixed induction of hepatic classical and alternative macrophage markers in mice fed EtOH-containing diet showed mixed induction of hepatic classical and alternative macrophage markers. In addition, EtOH significantly increased TERT in isolated KCs and RAW 264. 7 cells, and LPS-induced TERT production in vitro. In addition, loss- and gain-of-function studies showed that TERT converted macrophages toward M1 phenotype by regulating NF-B signaling, but had no effect on M2 macrophages polarization in vitro. According to our report, TERT plays a key role in macrophage polarization and M1 macrophage polarization.

Source link: https://doi.org/10.1038/srep18685


Association of CA 125 with Degree of Fibrosis in Chronic Liver Disease with Portal Hypertension

The aim: To determine the relationship between serum CA-125 levels and the degree of fibrosis in chronic liver disease with portal hypertension. A total of 63 patients with liver cirrhosis were enrolled, demographic, medical, and laboratory results were documented. CA-125 as a 50 IU/L was calculated using a receiver operating character curve to determine cut off value for CA-125. Pearson correlation and linear regression analysis were used to determine the relationship between CA-125 and modified fib -4 index. Female patients were 22 years old, and male patients were 41. Modified fib-4score was 4. 75-2. 8 percent, 43 had a value above cutoff of 3. 89 percent. This association was statistically significant for the CA-125 value above 50 IU/L's 63% sensitivity and 70% specificity in predicting advanced liver fibrosis. Conclusion: A corresponding serum CA-125 level above 50 IU/L is associated with significant liver fibrosis.

Source link: https://doi.org/10.21649/akemu.v27i4.4896


Key Signaling in Alcohol-Associated Liver Disease: The Role of Bile Acids

Alcohol-associated liver disease is a spectrum of disorders, the onset and progression of which are related to regular alcohol use. ALD continues to be a significant health risk and is now the leading cause of liver transplantations in the United States. Due to dietary disruption and gut dysbiosis in ALD, bile acid signaling and metabolism are also affected, as well as other liver disease disorders, such as non-alcoholic fatty liver disease.

Source link: https://doi.org/10.3390/cells11081374


Obesity Modifies the Performance of Fibrosis Biomarkers in Nonalcoholic Fatty Liver Disease

Abstract Context Guidelines encourage blood-based fibrosis biomarkers to detect advanced nonalcoholic fatty liver disease, which is particularly prevalent in obese patients. In NAFLD, the aim of the research was to determine if obesity influences liver fibrosis biomarkers' results. Patients from endocrinology and hepatology clinics undergoing a liver biopsy were recruited by patients with an elevated body mass index of 40. 3 kg/m2. [fibrotic nonalcoholic steatohepatitis] is a common measure of failure [fibrotic nonalcoholic steatohepatitis ] is a disease that causes respiratory fibrosis [fibrotic nonalcoholic steatohepatitis]. New cutoffs for NFS have been derived and tested to rule in/out fibrosis in groups with BMIs ranging from 30. 0, 30. 0 to 39. 9, and 40. 0 kg/m2. FIB-4 with ADAPT or FIBC3 gives more granularity to diagnosis fibrosis of a F3 sequence. BMI and the cheap FIB-4, the best-performing fibrosis biomarkers in obese patients, are ADAPT and FIB-4, which are unaffected by BMI.

Source link: https://doi.org/10.1210/clinem/dgab933

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions