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Chronic liver disease inevitably progresses to liver cirrhosis, significantly compromising patients' overall survival and quality of life. However, a glimmer of hope emerges with the emergence of mesenchymal stem cells, possessing remarkable abilities for self-renewal, differentiation, and immunomodulation. Leveraging their potential, MSCs have become a focal point in both basic and clinical trials, offering a promising therapeutic avenue to impede fibrosis progression and enhance the life expectancy of individuals battling hepatic cirrhosis. This comprehensive review serves to shed light on the origin of MSCs, the intricate mechanisms underlying cirrhosis treatment, and the cutting-edge advancements in basic and clinical research surrounding MSC-based therapies for liver cirrhosis patients. • Liver cirrhosis is the final stage of many chronic liver diseases. • Mesenchymal stem cells (MSCs) have paracrine, anti-fibrotic, anti-oxidative stress, and immunomodulatory effects, making them a potential treatment option for liver cirrhosis. • MSC-EVs, gene modification, hypoxia, preconditioning with cytokines or growth factors, and combination therapy can enhance the therapeutic effect of MSCs in treating liver cirrhosis. • Clinical trials have proven MSCs' safety and effectiveness in treating liver cirrhosis. [ABSTRACT FROM AUTHOR]

Chronic Liver fibrosis may progress to liver cirrhosis and hepatocellular carcinoma (HCC), hence cause a substantial global burden. However, effective therapies for blocking fibrosis are still lacking. Although mesenchymal stem cells (MSCs) have been proven beneficial to liver regeneration after damage, the underlying mechanism of their therapeutic effects are not fully understood. Oxidative stress and mitochondrial functionality alteration directly contributes to the hepatocyte apoptosis and development of liver fibrosis. This study aims to elucidate the mechanism by which hUC-MSC alleviates liver fibrosis and mitochondrial dysfunction. RNA-sequencing was performed to characterize the transcriptomic changes after implantation of hUC-MSCs in mice with liver fibrosis. Next, western blot, RT-PCR, immunohistochemical and immunofluorescence staining were used to evaluate the expression of different genes in vitro and in vivo. Additionally, mitochondrial morphological and dynamic changes, ROS content, and ATP production were examined. Slc25a47, a newly identified liver-specific mitochondrial NAD+ transporter, was notably reduced in CCl 4 -treated mice and H 2 O 2 -stimulated hepatocytes. Conversely, hUC-MSCs increased the Slc25a47 expression and NAD+ level within mitochondria, thereby enhanced Sirt3 protein activity and alleviated mitochondrial dysfunction in the liver. Furthermore, Slc25a47 knockdown could partially abrogate the protective effects of hUC-MSCs on H 2 O 2 -induced mitochondrial fission and oxidative stress in hepatocytes. Our study illustrates that Slc25a47 is a key molecular for hUC-MSCs to improve liver fibrosis and regulates mitochondrial function through Sirt3 for the first time, and providing a theoretical basis for the clinical translation of hUC-MSCs transplantation in the treatment of patients with liver fibrosis/cirrhosis. • hUC-MSCs transplantation alleviate mice liver fibrosis and improve liver function. • mitochondrial NAD+ transporter Slc25a47 was decreased under stressful conditions. • hUC-MSCs reduced hepatic oxidative stress and mitochondrial damage. • hUC-MSCs improve mitochondrial dysfunction via increasing Slc25a47 expression and protein activity of Sirt3. [ABSTRACT FROM AUTHOR]

Abstract: Background: Mallory–Weiss syndrome is defined by upper gastrointestinal bleeding from vomiting-induced mucosal lacerations at the esophago-gastric junction. This study was purposed to investigate the incidence, location, clinical manifestation, diagnosis and effectiveness of treatment (including endoscopic treatment and conservative medical treatment) of Mallory-Weiss syndrome in China. Methods: All patients who received emergency upper gastrointestinal endoscopy due to Mallory–Weiss syndrome from September 2007 to August 2011 at gastrointestinal endoscopy center of Renmin Hospital of Wuhan University were included in this study. The clinical presentation, medical history, location and characteristics of Mallory–Weiss syndrome methods and effectiveness of therapy of patients with Mallory–Weiss syndrome were retrospectively analyzed by chart reviews. Long-term follow-up data were collected at outpatient clinics or telephone interviews. Results: Sixteen patients were diagnosed with Mallory–Weiss syndrome, which account for 3.08% of 519 patients with acute non-variceal upper gastrointestinal bleeding. Common comorbidities were found in one patient with hepatic cirrhosis. Conservative medical treatment, local injection, hemoclipping, or multipolar electrocoagulation produced primary hemostasis in 87.5% (14/16) of patients. Conclusion: Mallory–Weiss syndrome is uncommon in China in comparison with reported experience in the west when the same group of patients is selected. Different approaches to treatment are to be recommended depending on whether or not active hemorrhage is present. [Copyright &y& Elsevier]