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LGR4 is a key regulator of hepatic gluconeogenesis.
Free Radic Biol Med
January 2025
Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Key Laboratory for Endocrine Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:
Aims/hypothesis: Emerging evidence underscored the significance of leucine-rich repeat-containing G protein-coupled receptor (LGR) 4 in endocrine and metabolic disorders. Despite this, its role in LGR4 in hepatic glucose metabolism remains poorly understood. In this study we set out to test whether LGR4 regulates glucose production in liver through a specific signaling pathway.
View Article and Find Full Text PDFGene therapy in polycystic kidney disease: A promising future.
J Transl Int Med
December 2024
Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), Shanghai 200003, China.
Polycystic kidney disease (PKD) is a genetic disorder marked by numerous cysts in the kidneys, progressively impairing renal function. It is classified into autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD), with ADPKD being more common. Current treatments mainly focus on symptom relief and slowing disease progression, without offering a cure.
View Article and Find Full Text PDFBNIP3 Downregulation Ameliorates Muscle Atrophy in Cancer Cachexia.
Cancers (Basel)
December 2024
Department of Clinical and Biological Sciences, University of Torino, 10043 Turin, Italy.
Background And Aims: Cancer cachexia is a complex syndrome affecting most cancer patients and is directly responsible for about 20% of cancer-related deaths. Previous studies showed muscle proteolysis hyper-activation and mitophagy induction in tumor-bearing animals. While basal mitophagy is required for maintaining muscle mass and quality, excessive mitophagy promotes uncontrolled protein degradation, muscle loss and impaired function.
View Article and Find Full Text PDFFhl1, a new spatially specific protein, regulates vein graft neointimal hyperplasia.
Clin Transl Med
December 2024
Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Article Synopsis
- Vein grafts are critical for treating coronary artery disease, but neointimal hyperplasia (NIH) poses a significant challenge to their long-term success, with current identification and intervention methods being insufficient.
- Researchers conducted a study using rats to observe the NIH development process after vein grafting while examining gene expression and specific markers related to NIH through various analytical methods.
- The results showed that repair cells from outside the graft contribute significantly to NIH, with the protein Fhl1 playing a protective role against inflammation and cell proliferation, offering potential targets for improved treatments.
[Nlrp6 overexpression inhibits lipid synthesis to suppress proliferation of hepatocellular carcinoma cells by regulating the AMPK-Srebp1c axis].
Nan Fang Yi Ke Da Xue Xue Bao
October 2024
Central Laboratory, First College of Clinical Medical Science of China Three Gorges University (Yichang Central People's Hospital)//Hubei Key Laboratory of Ischemic Cardiovascular Disease//Hubei Provincial Clinical Research Center for Ischemic Cardiovascular Disease, Yichang 443003, China.
Objective: To investigate the mechanism of Nlrp6 for regulating hepatocellular carcinoma (HCC) progression in light of lipid synthesis regulation.
Methods: Nlrp6 expression level in HCC tissues of different pathological grades was investigated using RNA-seq data from The Cancer Genome Atlas (TCGA) database, and its correlation with the patients' survival was analyzed with Kaplan-Meier survival analysis. HepG2 cells with adenovirus-mediated Nlrp6 overexpression or knockdown were treated with palmitic acid (PA), and the changes in lipid deposition and cell proliferation were evaluated using Oil Red O staining, CCK-8 assay, EdU staining, and colony formation assay.
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