ArticleActa pharmacologica Sinica2022
Transcription factor Klf9 controls bile acid reabsorption and enterohepatic circulation in mice via promoting intestinal Asbt expression.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Klf9 Loss of Function Protects Against Glucocorticoids Induced Skeletal Muscle Wasting.Journal of cachexia, sarcopenia and muscle · 2025Article
- Article
- Immune-metabolic interactions shape the fibrotic landscape of diabetic kidney disease: emerging mechanisms and therapeutic prospects.Frontiers in physiology · 2025Review
- Klf9 is essential for cardiac mitochondrial homeostasis.Nature cardiovascular research · 2024Article
- Intestinal flora and bile acid interactions impact the progression of diabetic kidney disease.Frontiers in endocrinology · 2024Review
- Review
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bile acid (BA) homeostasis is regulated by the extensive cross-talk between liver and intestine. Many bile-acid-activated signaling pathways have become attractive therapeutic targets for the treatment of metabolic disorders. In this study we investigated the regulatory mechanisms of BA in the intestine. We showed that the BA levels in the gallbladder and faeces were significantly increased, whereas serum BA levels decreased in systemic Krüppel-like factor 9 (Klf9) deficiency (Klf9
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Registered trials
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