Article
Cell Biology
Qi Wang, Song Wei, Lei Li, Qingfa Bu, Haoming Zhou, Wantong Su, Zheng Liu, Mingming Wang, Ling Lu
Summary: The study highlighted the regulatory role of lncRNA NEAT1 and miR-139-5p in liver fibrosis progression, with NEAT1 promoting HSCs activation by sponging miR-139-5p. The overexpression of miR-139-5p or knockdown of NEAT1 alleviated liver fibrosis in vivo by targeting the beta-catenin/SOX9/TGF-beta 1 pathway.
CELL DEATH DISCOVERY
(2021)
Article
Biotechnology & Applied Microbiology
Li Dong, Yumin Zheng, Xiaoguang Luo
Summary: This study focused on exploring the role of NEAT1 in Parkinson's disease (PD) and its effects on PD and related molecular mechanisms. The results showed that NEAT1 was involved in the development of PD, regulating cellular proliferation, apoptosis, and autophagy. Interfering with NEAT1 had potential therapeutic effects on PD by increasing the level of miR-107-5p.
Article
Biochemistry & Molecular Biology
Xiang Wei, Shan Xu, Liang Chen
Summary: Sevoflurane exacerbates neurotoxicity by inhibiting cell viability and promoting cell apoptosis, neuroinflammation, and ROS production. Neat1 is up-regulated in sevoflurane-treated cells, and its knockdown can improve sevoflurane-induced neurotoxicity. Through a ceRNA mechanism, it was found that Neat1 interacts with miR-298-5p to up-regulate Srpk1, ultimately contributing to sevoflurane-stimulated neurotoxicity.
NEUROCHEMICAL RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Yabin Li, Xirui Wang, Zhihuang Zhao, Jinxing Shang, Gang Li, Ruijian Zhang
Summary: NEAT1 plays an oncogenic role in glioma progression by promoting cell proliferation and interacting with miR-98-5p and BZW1. Inhibition of NEAT1 through the miR-98-5p/BZW1 pathway suppresses glioma cell proliferation in vivo. Targeting NEAT1/miR-98-5p/BZW1 may provide a novel therapeutic approach for glioma patients.
BIOSCIENCE REPORTS
(2021)
Article
Cell Biology
Yangwei Xu, Yanyan Li, Yue Qiu, Fei Sun, Guifang Zhu, Jingbo Sun, Guixing Cai, Wanmei Lin, Yun Fu, Hongmei Wu, Shanshan Jiang, Zhihui Wen, Feiyan Feng, Junjie Luo, Yuqin Yang, Qingling Zhang
Summary: NEAT1 is upregulated in most GC samples and is associated with poor prognosis. It promotes GC angiogenesis by competitively sponging miR-17-5p to activate the TGF beta/Smad pathway and upregulate proangiogenic factors like VEGF.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Cell Biology
Yang Yang, Jianhua Xue, Lili Qin, Jiaxuan Zhang, Jiajia Liu, Junbo Yu
Summary: NEAT1 inhibits the progression of sepsis induced by LPS in RAW264.7 cells by modulating the miR-31-5p/POU2F1 axis, suggesting NEAT1 as a potential therapeutic target for sepsis.
Article
Chemistry, Medicinal
Lu Wang, Xiaohui Wang, Lina Kong, Yingying Li, Kai Huang, Jingjing Wu, Changyuan Wang, Huijun Sun, Pengyuan Sun, Jiangning Gu, Haifeng Luo, Kexin Liu, Qiang Meng
Summary: Nonalcoholic fatty liver disease (NAFLD), a metabolic disease, currently lacks effective drugs for treatment. This study found that isoliquiritigenin (ISL) significantly improved liver histopathological changes caused by NAFLD by modulating miR-138-5p/PGC-1 alpha-mediated lipid metabolism and inflammatory reaction.
PHYTOTHERAPY RESEARCH
(2022)
Article
Biotechnology & Applied Microbiology
Juan Xiang, Yuan-Yuan Deng, Hui-Xia Liu, Ying Pu
Summary: This study explored the mechanism by which long non-coding RNA (lncRNA) MALAT1 regulates nonalcoholic fatty liver disease (NAFLD). It was found that MALAT1 is up-regulated in NAFLD and its knockdown suppressed lipid accumulation in hepatocytes induced by free fatty acids. MALAT1 regulates hepatic lipid accumulation in NAFLD through the miR-206/ARNT axis, which in turn affects the expression of PPAR alpha/CD36. Therefore, MALAT1 may serve as a potential therapeutic target against NAFLD.
FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY
(2022)
Article
Environmental Sciences
Yun Zhao, Ying Liu, Xue Shi
Summary: This study identified that lncRNA AC012360.1 is upregulated in hepatocellular carcinoma (HCC) tissues and promotes HCC progression by sponging miR-139-5p and upregulating LPCAT1 expression.
ENVIRONMENTAL TOXICOLOGY
(2023)
Article
Oncology
Fang-Yi Yao, Cui Zhao, Fang-Min Zhong, Ting-Yu Qin, Fang Wen, Mei-Yong Li, Jing Liu, Bo Huang, Xiao-Zhong Wang
Summary: This study reveals a novel METTL3/NEAT1/miR-766-5p/CDKN1A axis that plays a critical role in the progression of CML. NEAT1 expression is decreased in CML cell lines and PBMCs of CML patients, with METTL3-mediated m6A modification influencing its aberrant expression. MiR-766-5p, upregulated in CML PBMCs, interferes with the effects of NEAT1 on CML cell viability and apoptosis.
FRONTIERS IN ONCOLOGY
(2021)
Article
Biochemistry & Molecular Biology
L. Dong, Yumin Zheng, Lianbo Gao, Xiaoguang Luo
Summary: The study found that NEAT1 levels were significantly correlated with MPTP-induced Parkinson's disease (PD) mice, dopamine neurons, and cells treated with MPP+, and that NEAT1 inhibition effectively promoted cell proliferation, inhibited apoptosis and autophagy. Silencing NEAT1 increased the TH+ rate of neurons and greatly suppressed autophagy. Additionally, NEAT1 may impact apoptosis and autophagy of SH-SY5Y cells through miR-374c-5p.
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
(2021)
Article
Cell Biology
Yan Xie, Li Rong, Min He, Yuyou Jiang, Haiyu Li, Li Mai, Fangzhou Song
Summary: High expression of SNHG3 in gastric cancer is correlated with tumor clinical stage and patient survival rate, while knocking down SNHG3 can inhibit the proliferation, migration, and invasion of GC cells. SNHG3 binds and sequesters miR-139-5p to indirectly promote the upregulation of the miR139-5p target gene MYB, driving the oncogenic activities of GC.
Article
Cell Biology
Min-Jie Hu, Mei Long, Rong-Juan Dai
Summary: Non-alcoholic fatty liver disease (NAFLD) is a global health burden, and the regulatory mechanisms involving H3K27 acetylation, lncRNA NEAT1, miR-212-5p, and GRIA3 in NAFLD were investigated. Upregulation of NEAT1 and GRIA3, and downregulation of miR-212-5p were observed in NAFLD patients. Fatty acid treatment promoted NEAT1 and GRIA3 expression, suppressed miR-212-5p expression, and led to lipid accumulation.
MOLECULAR AND CELLULAR BIOCHEMISTRY
(2022)
Article
Environmental Sciences
Han Li, Lu Wu, Fuping Ye, Dapeng Wang, Li Wang, Wenqi Li, Yuan Xu, Zhenyang Li, Jingshu Zhang, Suhua Wang, Aihua Zhang, Qizhan Liu
Summary: Chronic exposure to arsenic disrupts fatty acid and methionine metabolism, leading to the development of nonalcoholic fatty liver disease (NAFLD). Arsenic blocks the maturation of miR-142-5p mediated by m6A by consuming S-adenosylmethionine (SAM) via As3MT, thereby increasing the levels of SREBP1 and lipogenic genes, resulting in NAFLD.
SCIENCE OF THE TOTAL ENVIRONMENT
(2023)
Article
Pharmacology & Pharmacy
Suwen Chen, Shangwen Sun, Yanan Feng, Xiu Li, Guoliang Yin, Pengpeng Liang, Wenfei Yu, Decheng Meng, Xin Zhang, Hongshuai Liu, Fengxia Zhang
Summary: Nonalcoholic fatty liver disease (NAFLD) is a common liver disease without approved treatment. Hepatic farnesoid X receptor (FXR) is a potential therapeutic target for NAFLD. Diosgenin (DG), a natural compound from Chinese herbal medicine, effectively prevents metabolic diseases. Our research reveals that DG can alleviate NAFLD by regulating the hepatic FXR-SHP-SREBP1C/PPARa/CD36 pathway.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2023)
Article
Gastroenterology & Hepatology
Fakhar Ali Qazi Arisar, Rhea Varghese, Shiyi Chen, Wei Xu, Markus Selzner, Ian Mcgilvray, Blayne Sayed, Trevor Reichman, Chaya Shwaartz, Mark Cattral, Anand Ghanekar, Gonzalo Sapisochin, Elmar Jaeckel, Cynthia Tsien, Nazia Selzner, Leslie Lilly, Mamatha Bhat
Summary: Recurrent cirrhosis complicates a significant percentage of liver transplants and may require re-transplantation. This study examined the trajectories of relisted versus primary listed patients on the waitlist and assessed their overall survival and cumulative incidence of transplant.
ANNALS OF HEPATOLOGY
(2024)
Article
Gastroenterology & Hepatology
Helena Hernandez-Evole, Natalia Jimenez-Esquivel, Elisa Pose, Ram on Bataller
Summary: Alcohol is the leading cause of preventable morbidity and mortality worldwide, and the most frequent cause of liver disease. Alcohol-associated liver disease has a complex pathogenesis, with unknown precise mechanisms. Currently, there are no targeted therapies to interfere with the disease's progression, making alcohol abstinence the most effective measure to improve prognosis in patients with this disease.
ANNALS OF HEPATOLOGY
(2024)
Letter
Gastroenterology & Hepatology
Alexander M. Sy
ANNALS OF HEPATOLOGY
(2024)
Letter
Gastroenterology & Hepatology
Eric David Ornos, Janus P. Ong
ANNALS OF HEPATOLOGY
(2024)
Review
Gastroenterology & Hepatology
Lauren Loeb, Jason Lewis, Zhongwei Peng, Michael G. Heckman, Raouf Nakhleh, Andrew P. Keaveny
Summary: Congenital hepatic fibrosis (CHF) is a rare condition characterized by biliary tract changes and liver fibrosis. This study reviewed the medical records of 24 adult patients with CHF and found that renal cysts, splenomegaly, and a cirrhotic-appearing liver were the most common imaging findings. The most common liver-related complications were cholangitis, varices, and hepatic encephalopathy. Liver transplantation may be required for patients with decompensated disease.
ANNALS OF HEPATOLOGY
(2024)