Publications by authors named "Teja Naveen Sata"
Introduction And Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the primary causes of chronic liver disease and may lead to liver cirrhosis and hepatocellular carcinoma. Recent reports suggested that DEAD-box RNA helicase (DDX3) acts as a sensor of free fat accumulation and may modulate the pathogenesis via miRNAs. Hence, we hypothesized that DDX3 might modulate MASLD progression via miRNA-141-mediated inhibition of Sirt-1 and autophagy.
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- Non-alcoholic fatty liver disease (NAFLD) is a major global health issue that can progress to more serious conditions like non-alcoholic steatohepatitis (NASH) and liver cancer (HCC), but the underlying molecular mechanisms are still not fully understood.
- This study focuses on how microRNA-122 regulates pyruvate kinase M2 (PKM2) and its impact on inflammatory and autophagic proteins during NAFLD development using both cell cultures and animal models.
- Results indicate that free fatty acids (FFAs) reduce miR-122 levels, leading to increased PKM2 and inflammation while suppressing proteins related to autophagy, highlighting the complex interactions that contribute to NA
HBV entry to the host cells and its successful infection depends on its ability to modulate the host restriction factors. DEAD box RNA helicase, DDX3, is shown to inhibit HBV replication. However, the exact mechanism of inhibition still remains unclear.
View Article and Find Full Text PDFHepatitis B virus (HBV) infection targets host restriction factors that inhibit its replication and survival. Previous studies have shown that barriers to autointegration factor1 (BANF1) inhibited the replication of herpes simplex virus and vaccinia virus by binding to phosphate backbone of dsDNA. To date, no reports are available for the interplay between BANF1 and HBV.
View Article and Find Full Text PDFAims: Non-alcoholic fatty liver disease is one of the major health concerns in the World. The dietary free fatty acids (FFAs) affect the metabolic status of the hepatocytes by modulating cellular pathways. In this study, we showed that free fatty acids stimulate apoptosis by upregulating miR-181a-5p expression, which in turn targets XIAP and Bcl2.
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- The study investigates the role of Augmenter of liver regeneration (ALR) and microRNA-26a in liver cell proliferation, specifically using the Huh7 cell line and mesenchymal stem cells from patients with chronic liver disease and healthy individuals.
- Findings indicate that overexpression of ALR or miRNA-26a enhances cell proliferation by activating the Akt signaling pathway and cyclin D1, while inhibiting ALR or miRNA-26a reduces this proliferation.
- The research concludes that ALR boosts miRNA-26a expression, which in turn suppresses phosphatase and tensin homolog, promoting cell proliferation through the Akt/cyclin D1 pathway in liver cells.
Objective: To study the role of miRNA-181a and augmenter of liver regeneration in TGF-β-induced fibrosis in hepatic stellate cells.
Methods: LX2 cells were treated with 20 ng/ml TGF-β for 24 h. miRNA-181a, ALR plasmid and empty vectors were transfected using siPORT NeoFx reagent.