CREBH promotes autophagy to ameliorate NASH by regulating Coro1a.

Dysfunctional autophagy aggravates oxidative stress and inflammation in hepatocytes and accelerates the progression of nonalcoholic steatohepatitis (NASH). Here, we demonstrated that cAMP-responsive element-binding protein H (CREBH) is a transcriptional regulator of hepatic autophagy in response to diet-induced NASH. The results showed that the upregulation of CREBH in lipid-overloaded hepatocytes improves cell damage, dysfunction of autophagic flux and associated abnormal accumulation of the autophagosome marker LC3-II and autophagic substrate p62.

Exploration of Perturbed Liver Fibrosis-Related Factors and Collagen Type I in Animal Model of Non-Alcoholic Fatty Liver Disease.

To determine their involvement in the onset of the disease, we investigated the changing levels of liver fibrosis-related proteins, namely, type-I collagen, α-smooth muscle actin (α-SMA), and transforming growth factor β1 and β3 (TGF-β1, β3). The four groups of Sprague-Dawley (SD) rats were involved in the study, namely, (i) normal control group, (ii) high-fat diet group (HFD), (iii) carbon tetrachloride (CCl) group, and (iv) NAFLD group (animal model) which were chosen at random. The NAFLD model received HFD combined with subcutaneous injection of small doses of CCl.

Intestinal BMP-9 locally upregulates FGF19 and is down-regulated in obese patients with diabetes.

Bone morphogenetic protein (BMP)-9, a member of the TGFβ-family of cytokines, is believed to be mainly produced in the liver. The serum levels of BMP-9 were reported to be reduced in newly diagnosed diabetic patients and BMP-9 overexpression ameliorated steatosis in the high fat diet-induced obesity mouse model. Furthermore, injection of BMP-9 in mice enhanced expression of fibroblast growth factor (FGF)21.

Difference between type 2 gastroesophageal varices and isolated fundic varices in clinical profiles and portosystemic collaterals.

Background: There is significant heterogeneity between gastroesophageal varices (GOV2) and isolated gastric varices (IGV1). The data on the difference between GOV2 and IGV1 are limited.

Aim: To determine the etiology, clinical profiles, endoscopic findings, imaging signs, portosystemic collaterals in patients with GOV2 and IGV1.

Prevalence and impact of Sjögren's syndrome in primary biliary cholangitis: a systematic review and meta-analysis.

Introduction And Objectives: We performed a systematic review and meta-analysis to evaluate the prevalence of concomitant Sjögren's syndrome (SS) with primary biliary cholangitis (PBC) in adults and quantify the impact of SS on PBC.

Methods: PubMed, Web of Science and Cochrane library were searched using subject terms and predefined inclusion and exclusion criteria.

Results: Seventeen articles were included.

CREBH alleviates mitochondrial oxidative stress through SIRT3 mediating deacetylation of MnSOD and suppression of Nlrp3 inflammasome in NASH.

Lipotoxicity and unresolved oxidative stress are key drivers of metabolic inflammation in nonalcoholic steatohepatitis (NASH). cAMP-response element binding protein H(CREBH) is a liver-specific transcription factor and regulates the glucose and lipid metabolism of NASH. However, its role in mitochondrial oxidative stress and its association with sirtuin 3 (SIRT3), a master regulator of deacetylation for mitochondrial proteins, remains elusive.

The Role and Mechanism of CREBH Regulating SIRT3 in Metabolic Associated Fatty Liver Disease.

Aims: To investigate the effect of cAMP response element-binding protein H (CREBH) on metabolic associated fatty liver disease by regulating sirtuin 3 (SIRT3).

Main Methods: Two mouse models of fatty liver induced by a methionine-choline deficient (MCD) diet and a high-fat (HF) diet and an in vitro model of palmitic acid (PA) induced lipid-overloaded hepatocytes were constructed to detect the expression of CREBH, SIRT3, total acetylation, and downstream protein interactions and lipid metabolism phenotype, which were further validated in CREBH mice and lentivirus-overexpressing CREBH hepatocytes.

Key Findings: In fatty liver and lipid overload models, the expressions of CREBH and SIRT3 were down-regulated and their expression was positively correlated, accompanied by an increase in the level of total protein acetylation.

Resolvin D1 attenuates CCl4 Induced Liver Fibrosis by Inhibiting Autophagy-Mediated HSC activation AKT/mTOR Pathway.

Resolvin D1 (RvD1) was previously reported to relieve inflammation and liver damage in several liver diseases, but its potential role in liver fibrosis remains elusive. The aim of our study was to investigate the effects and underlying mechanisms of RvD1 in hepatic autophagy in liver fibrosis. , male C57BL/6 mice were intraperitoneally injected with 20% carbon tetrachloride (CCl4, 5 ml/kg) twice weekly for 6 weeks to establish liver fibrosis model.

Zhikang Capsule Ameliorates Inflammation, Drives Polarization to M2 Macrophages, and Inhibits Apoptosis in Lipopolysaccharide-induced RAW264.7 Cells.

Objective: To explore the anti-inflammatory effect of the traditional Chinese medicine Zhikang capsule (ZKC) on lipopolysaccharide (LPS)-induced RAW264.7 cells.

Methods: Safe concentrations of ZKC (0.

Identification and Validation of a Nine-Gene Amino Acid Metabolism-Related Risk Signature in HCC.

Hepatocellular carcinoma (HCC) is the world's second most deadly cancer, and metabolic reprogramming is its distinguishing feature. Among metabolite profiling, variation in amino acid metabolism supports tumor proliferation and metastasis to the most extent, yet a systematic study on the role of amino acid metabolism-related genes in HCC is still lacking. An effective amino acid metabolism-related prediction signature is urgently needed to assess the prognosis of HCC patients for individualized treatment.

New insights into BMP9 signaling in liver diseases.

Bone morphogenetic protein 9 (BMP9) is a recently discovered cytokine mainly secreted by the liver and is a member of the transforming growth factor β (TGF-β) superfamily. In recent years, an increasing number of studies have shown that BMP9 is associated with liver diseases, including nonalcoholic fatty liver disease (NAFLD), liver fibrosis and hepatocellular carcinoma (HCC), and BMP9 signaling may play dual roles in liver diseases. In this review, we mainly summarized and discussed the roles and potential mechanisms of BMP9 signaling in NAFLD, liver fibrosis and HCC.

BMP9 promotes methionine- and choline-deficient diet-induced nonalcoholic steatohepatitis in non-obese mice by enhancing NF-κB dependent macrophage polarization.

Our previous study confirmed that bone morphogenetic protein 9 (BMP9) participated in the development of nonalcoholic steatohepatitis (NASH) by affecting macrophage polarization. The focus of this study was to further confirm the role of macrophages in BMP9-mediated NASH and to analyze the underlying mechanism. In vivo, mice that were administered adeno-associated viral (AAV) vectors containing a null transgene (AAV-null) or the BMP9 transgene (AAV-BMP9) were divided into methionine- and choline-deficient (MCD) and control diet (CD) groups, and they were administered either control liposomes or clodronate liposomes via tail vein injection, the latter to deplete macrophages.

Resolvin D1 mitigates non-alcoholic steatohepatitis by suppressing the TLR4-MyD88-mediated NF-κB and MAPK pathways and activating the Nrf2 pathway in mice.

Aims: Resolvin D1 (RvD1), a potent endogenous lipid mediator converted from docosahexaenoic acid (DHA), has exert anti-inflammatory and antioxidant effects in many preclinical disease models, but its potential role in non-alcoholic steatohepatitis (NASH) remains elusive. This study was performed to investigate the protective effects and mechanisms of RvD1 in NASH.

Main Methods: In vivo, male C57BL/6 mice were fed an MCD diet for 4 weeks to induce NASH.

N-glycosylation of CREBH improves lipid metabolism and attenuates lipotoxicity in NAFLD by modulating PPARα and SCD-1.

Introduction: Cyclic adenosine monophosphate (AMP)-responsive element-binding protein H (CREBH), an endoplasmic reticulum-anchored transcription factor essential for lipid metabolism and inflammation in nonalcoholic fatty liver disease (NAFLD), is covalently modified by N-acetylglucosamine. Glycosylation is a ubiquitous type of protein involved in posttranslational modifications, and plays a critical role in various biological processes. However, the mechanism of glycosylated CREBH remains poorly understood in NAFLD.

Clinical application of carbon nanoparticles in lymphatic mapping during colorectal cancer surgeries: A systematic review and meta-analysis.

Objective: To investigate the overall performance of carbon nanoparticles (CNs) for detecting lymph nodes (LNs) and node metastasis during colorectal cancer surgery.

Methods: The English and Chinese literature was searched until 29 April 2020. Studies were included if they were randomized controlled trials (RCTs) for colorectal resection and LN dissection that compared the use of CNs with a blank control in colorectal cancer surgery.

Advances in characterization of SIRT3 deacetylation targets in mitochondrial function.

The homeostasis of mitochondrial functional state is intimately in relation with SIRT3 (sirtuin3). SIRT3, the deacetylase mainly anchored in mitochondria, acts as a modulator of metabolic regulation via manipulating the activity and function of downstream targets at post-translational modification levels. The features of energy sensing and ADP-ribose transference of SIRT3 have also been reported.

Blood biochemical characteristics of patients with coronavirus disease 2019 (COVID-19): a systemic review and meta-analysis.

Objective Recently, there have been several studies on the clinical characteristics of patients with coronavirus disease 2019 (COVID-19); however, these studies have mainly been concentrated in Wuhan, China; the sample sizes of each article were different; and the reported clinical characteristics, especially blood biochemical indices, were quite different. This study aimed to summarize the blood biochemistry characteristics of COVID-19 patients by performing a systemic review and meta-analysis of published studies. Methods Comprehensive studies were screened from PubMed, Embase, and Cochrane Library through March 11, 2020.

CREBH knockout accelerates hepatic fibrosis in mouse models of diet-induced nonalcoholic fatty liver disease.

Aims: The primary focus of this study was to explore the effects of cyclic AMP response element-binding protein H (CREBH) on the development of nonalcoholic fatty liver disease (NAFLD).

Materials And Methods: CREBH knockout (KO) and wildtype (WT) mice were averagely divided into a methionine and choline-deficient (MCD) or high fat (HF) diet group and respective chow diet (CD) groups. Mice were sacrificed after 4-week treatment for MCD model and 24-week treatment for HF model.

Scoparone improves hepatic inflammation and autophagy in mice with nonalcoholic steatohepatitis by regulating the ROS/P38/Nrf2 axis and PI3K/AKT/mTOR pathway in macrophages.

Background And Aims: Scoparone has been shown to ameliorate many forms of liver disease, and several underlying molecular mechanisms involved have been previously revealed. However, the potential role of scoparone in autophagy, which is dysregulated in nonalcoholic fatty liver disease-nonalcoholic steatohepatitis (NAFLD-NASH), has not been evaluated. In the current study, we investigated the effect and potential mechanisms of scoparone in hepatic autophagy in mice with NASH.

The association of two common polymorphisms in miRNAs with diabetes mellitus: A meta-analysis.

Background: MicroRNAs (miRNAs) are small noncoding single-stranded RNAs with a length of ∼21 nucleotides. Single nucleotide polymorphisms (SNPs) may affect the function of miRNAs, resulting in a variety of disorders in vivo. Recently, diabetes mellitus (DM) has become a global healthcare problem, and several studies have reported that 2 common polymorphisms (miRNA 146a rs2910164 and miRNA 27a rs895819) are related to susceptibility to diabetes.

Scoparone alleviates inflammation, apoptosis and fibrosis of non-alcoholic steatohepatitis by suppressing the TLR4/NF-κB signaling pathway in mice.

Scoparone, a naturally-occurring, bioactive compound isolated from the Chinese herb Artemisia capillaria, has been shown to ameliorate hepatotoxicity and cholestasis in liver diseases. However, the pharmacological effect of scoparone in non-alcoholic steatohepatitis (NASH) has not been elucidated. In this study, we investigated the protective effects and mechanisms of scoparone in NASH.

Adenovirus‑mediated overexpression of bone morphogenetic protein‑9 promotes methionine choline deficiency‑induced non‑alcoholic steatohepatitis in non‑obese mice.

Liver inflammation and macrophage infiltration are critical steps in the progression of non‑alcoholic fatty liver to the development of non‑alcoholic steatohepatitis. Bone morphogenetic protein‑9 is a cytokine involved in the regulation of chemokines and lipogenesis. However, the function of bone morphogenetic protein‑9 in non‑alcoholic steatohepatitis is still unknown.

Ascitic fluid total protein, a useful marker in non-portal hypertensive ascites.

Background And Aims: Diagnostic performance of ascitic fluid total protein (AFTP) concentration remained unsettled. Our aim was to determine diagnostic value of AFTP in differential diagnosis of causes of ascites.

Methods: Seven hundred four consecutive patients with new-onset ascites were prospectively enrolled in this study.

Diallyl disulfide attenuates non‑alcoholic steatohepatitis by suppressing key regulators of lipid metabolism, lipid peroxidation and inflammation in mice.

Non‑alcoholic steatohepatitis (NASH) is a common clinicopathological condition. Currently, the pathogenesis of NASH remains unknown, and no optimal therapy option currently exists. It has previously been demonstrated that diallyl disulfide (DADS) was capable of attenuating liver dysfunction, as DADS supplementation had a positive impact on liver regeneration, proliferation and oxidative damage.