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The m6A demethylase ALKBH5 is a novel epigenetic regulator of aortic valve calcification.
Cardiovasc Res
December 2024
Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 510260, China.
Aims: Calcific aortic valve disease (CAVD) is a common heart valve disease with significant clinical consequences. The mechanisms that drive the pathogenesis of CAVD remain to be fully elucidated. N6-methyladenosine (m6A), the most prevalent RNA epigenetic regulator, has recently been implicated in cardiovascular disease, but its role in CAVD has yet to be investigated.
View Article and Find Full Text PDFRoles of mA modification in regulating PPER pathway in cadmium-induced pancreatic β cell death.
Ecotoxicol Environ Saf
September 2024
Institute of Preventive Medicine, School of Public Health, Dali University, No. 22, Wanhua Road, Dali, Yunnan 671000, People's Republic of China. Electronic address:
Cadmium can lead to the death of pancreatic β cells, thus affecting the synthesis and secretion of insulin. However, the specific mechanisms underlying the cadmium-induced pancreatic β cell death have not been fully understood. In this study, roles of mA modification in regulating protein processing in endoplasmic reticulum (PPER) pathway in cadmium-induced pancreatic β cell death were explored.
View Article and Find Full Text PDFlinc01515 regulates PM-induced oxidative stress via targeting NRF2 in airway epithelial cells.
Environ Pollut
August 2023
Department of Environmental Genomics, Institute of Healthy Jiangsu Development, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China; Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, Center of Global Health, School of Public Health, Nanjing Medical University, Nanjing, China. Electronic address:
Dysregulation of long non-coding RNAs (lncRNAs) is involved in the adverse effects caused by fine particulate matter (PM). However, the molecular mechanism is not fully clarified. In this study, we performed lncRNA sequencing on PM-treated human bronchial epithelial (HBE) cells to identify vital lncRNAs, and verified the differential expression of the lncRNAs by RT-qPCR in HBE and human normal lung epithelial (BEAS-2B) cells.
View Article and Find Full Text PDFlncRNA ZNRD1-AS1 promotes malignant lung cell proliferation, migration, and angiogenesis via the miR-942/TNS1 axis and is positively regulated by the mA reader YTHDC2.
Mol Cancer
December 2022
School of Public Health, Suzhou Medical College of Soochow University, Suzhou, 215123, Jiangsu, China.
Rationale: Lung cancer is the most prevalent form of cancer and has a high mortality rate, making it a global public health concern. The N-methyladenosine (mA) modification is a highly dynamic and reversible process that is involved in a variety of essential biological processes. Using in vitro, in vivo, and multi-omics bioinformatics, the present study aims to determine the function and regulatory mechanisms of the long non-coding (lnc)RNA zinc ribbon domain-containing 1-antisense 1 (ZNRD1-AS1).
View Article and Find Full Text PDFElevated S-adenosylhomocysteine induces adipocyte dysfunction to promote alcohol-associated liver steatosis.
Sci Rep
July 2021
Research Service (151), Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Avenue, Omaha, NE, 68105, USA.
It has been previously shown that chronic ethanol administration-induced increase in adipose tissue lipolysis and reduction in the secretion of protective adipokines collectively contribute to alcohol-associated liver disease (ALD) pathogenesis. Further studies have revealed that increased adipose S-adenosylhomocysteine (SAH) levels generate methylation defects that promote lipolysis. Here, we hypothesized that increased intracellular SAH alone causes additional related pathological changes in adipose tissue as seen with alcohol administration.
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