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Type 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.
Burns Trauma
January 2025
Department of Critical Care Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No. 321 Zhongshan Road, Gulou District, Nanjing, Jiangsu 210008, China.
Background: Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.
View Article and Find Full Text PDFThyroid Endocrine Disrupting Potential of Fluoxetine in Zebrafish Larvae.
J Appl Toxicol
January 2025
Changjiang Basin Ecology and Environment Monitoring and Scientific Research Center, Changjiang Basin Ecology and Environment Administration, Ministry of Ecology and Environment, Wuhan, China.
Fluoxetine (FLX), a typical selective serotonin reuptake inhibitors, has been frequently detected in aquatic environment and wild fish. However, little is known about its effect on thyroid endocrine system. In the present study, zebrafish (Danio rerio) embryos were exposed to 1, 3, 10, and 30 μg/L of FLX for 6 days.
View Article and Find Full Text PDFNitrate induced hepatic fibrosis in tadpoles of Bufo gargarizans by mediating alterations in toll-like receptor signaling pathways.
Environ Res
January 2025
Life and Environmental Science College, Wenzhou University, 325003, Wenzhou, China; Zhejiang Provincial Key Laboratory for Subtropical Water Environment and Marine Biological Resources Protection, Wenzhou University, 325003, Wenzhou, China. Electronic address:
The nitrate pollution has become an increasingly serious environmental problem worldwide, and the toxic effects of elevated nitrate levels in the environment on aquatic animals remain to be elucidated. The purpose of the present study was to investigate the mechanisms of liver injury to tadpoles after exposure to nitrate from embryonic to metamorphic climax and to assess the recovery process of liver function after cessation of exposure. In the group with continuous nitrate exposure, the livers and thyroid of tadpoles showed remarkably histological lesions, of this with structural disorganization of the hepatocytes, cellular atrophy, and fibrosis, as well as significant reduction in the follicular and colloidal area of the thyroid.
View Article and Find Full Text PDFAssociation between epigenome-wide DNA methylation changes and early neurodevelopment in preschool children: Evidence from a former impoverished county in Central China.
Gene
January 2025
Department of Maternal and Child Health School of Public Health Tongji Medical College Huazhong University of Science and Technology Wuhan China; Key Laboratory of Environment and Health, Ministry of Education and Ministry of Environmental Protection, State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, Hubei 430030, China. Electronic address:
Background: Existing epigenome-wide association study (EWAS) investigating the association between DNA methylation (DNAm) and child neurodevelopment have been predominantly conducted within Western populations, and yielded inconsistent results, leading to a significant gap within non-Western setting, particularly in resource-limited rural areas of Central China.
Objectives: To investigate the association between altered epigenome-wide DNAm and neurodevelopment in preschool children from resource-limited rural areas of Central China.
Methods: This case-control study involved 64 preschoolers.
Development of animal models to study aggressive thyroid cancers.
Eur Thyroid J
January 2025
J Knauf, Center for Immunotherapy and Precision Immuno-Oncology, Cleveland Clinic, Cleveland, United States.
The development of mouse models for thyroid cancer has significantly advanced over the years, enhancing our understanding of thyroid tumorigenesis, molecular pathways, and treatment responses. The earliest mouse models of thyroid cancer relied on hormone, radiation, or chemical carcinogenesis to induce tumors. However, as our understanding of the genetic alterations driving thyroid cancer has expanded, more sophisticated genetic engineering techniques have been employed to create models with thyroid-specific expression of these driver mutations.
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