ArticleBiochemical and biophysical research communications2014
Thyroid hormone status regulates the expression of secretory phospholipases.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Transcriptomic Features of Thyroid Signaling Disorders in Experimental Pulmonary Arterial Hypertension.Bulletin of experimental biology and medicine · 2026Article
- Unbalanced long-chain fatty acid beta-oxidation in newborns with cystic fibrosis and congenital hypothyroidism.Molecular genetics and metabolism reports · 2025Article
- Human iPSC-based disease modeling studies identify a common mechanistic defect and potential therapies for AMD and related macular dystrophies.Developmental cell · 2024Article
- Untargeted lipidomic analysis and network pharmacology for parthenolide treated papillary thyroid carcinoma cells.BMC complementary medicine and therapies · 2023Article
- Novel mechanisms underlying inhibition of inflammation-induced angiogenesis by dexamethasone and gentamicin via PI3K/AKT/NF-κB/VEGF pathways in acute radiation proctitis.Scientific reports · 2022Article
- Secretory Phospholipase A2s in Insulin Resistance and Metabolism.Frontiers in endocrinology · 2021Review
- Thyroid hormones in diabetes, cancer, and aging.Aging cell · 2020Review
- Hypothyroidism-Induced Nonalcoholic Fatty Liver Disease (HIN): Mechanisms and Emerging Therapeutic Options.International journal of molecular sciences · 2020Review
- Secretory phospholipase AJournal of lipid research · 2017Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Thyroid hormone (T3) stimulates various metabolic pathways and the hepatic actions of T3 are mediated primarily through the thyroid hormone receptor beta (TRβ). Hypothyroidism has been linked with low grade inflammation, elevated risk of hepatic steatosis and atherosclerosis. Secretory phospholipases (sPLA2) are associated with inflammation, hyperlipidemia and atherosclerosis. Due to potential linkage between thyroid hormone and sPLA2, we investigated the effect of thyroid hormone status on the regulation of secretory phospholipases in mice, rats and human liver. T3 suppressed the expression of the sPLA2 group IIa (PLA2g2a) gene in the liver of BALB/c mice and C57BL/6 transgenic mice expressing the human PLA2g2a. PLA2g2a was elevated with hypothyroidism and high fat diets which may contribute to the low grade inflammation associated with hypothyroidism and diet induced obesity. We also examined the effects of the TRβ agonist eprotirome on hepatic gene regulation. We observed that eprotirome inhibited the expression of selected sPLA2 genes and furthermore the cytokine mediated induction PLA2g2a was suppressed. In addition, eprotirome induced genes involved in fatty acid oxidation and cholesterol clearance while inhibiting lipogenic genes. Our results indicate that in vivo thyroid hormone status regulates the abundance of sPLA2 and the inhibition of PLA2g2a by T3 is conserved across species. By regulating sPLA2 genes, T3 may impact processes associated with atherosclerosis and inflammation and TRβ agonists may ameliorate inflammation and hyperlipidemia.
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