ArticleFrontiers in physiology2019
Caveolin-1 Impacts on TGF-β Regulation of Metabolic Gene Signatures in Hepatocytes.
Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Age-related and postmenopausal breast cancer progression and treatment management: The significance of pro-inflammatory cytokines and CXC chemokines.Genes & diseases · 2025Review
- Dual signaling pathways of TGF-β superfamily cytokines in hepatocytes: balancing liver homeostasis and disease progression.Frontiers in pharmacology · 2025Review
- Retinoic acid generates a beneficial microenvironment for liver progenitor cell activation in acute liver failure.Hepatology communications · 2024Article
- Caveolin-1 is critical for hepatic iron storage capacity in the development of nonalcoholic fatty liver disease.Military Medical Research · 2023Article
- Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation.Nature communications · 2022Article
- Serum Caveolin-1 Level is Inversely Associated with Serum Vaspin, Visfatin, and HbA1c in Newly Diagnosed Men with Type-2 Diabetes.Reports of biochemistry & molecular biology · 2022Article
- Article
- Caveolin-1 Regulates Cellular Metabolism: A Potential Therapeutic Target in Kidney Disease.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolin-1 (CAV1) is a membrane protein associated with metabolism in various cell types. The transforming growth factor beta (TGF-β) is a pro-fibrogenic cytokine in the liver, but its metabolic gene signatures remain unclear to date. We have previously shown that CAV1 alters TGF-β signaling and blocks its pro-apoptotic function. Here, we defined TGF-β-induced metabolic gene signatures in hepatocytes and assessed whether CAV1 abundance affects TGF-β control of those metabolic genes. Microarray analyses of primary hepatocytes after TGF-β stimulation (48 h) showed differential expression of 4224 genes, of which 721 are metabolic genes (adjusted
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Registered trials
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