ArticleScientific reports2015
Simultaneous bile duct and portal vein ligation induces faster atrophy/hypertrophy complex than portal vein ligation: role of bile acids.
Article in Scientific reports, 2015. 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, 9 citations in OpenAlex.
- Sodium taurocholate promotes liver regeneration after portal vein ligation in rats.Scientific reports · 2025Article
- Bile Acid Overload Induced by Bile Duct and Portal Vein Ligation Improves Survival after Staged Hepatectomy in Rats.Current medical science · 2023Article
- Totally laparoscopic associating simultaneous bile duct and portal vein ligation for planned hepatectomy for primary liver cancer: a case report.Journal of medical case reports · 2023Article
- The Role of Farnesoid X Receptor in Accelerated Liver Regeneration in Rats Subjected to ALPPS.Current oncology (Toronto, Ont.) · 2021Article
- Additional partial hepatectomy at the time of portal vein ligation accelerates the regeneration of the future liver remnant.Scientific reports · 2021Article
- Hepatectomy-Induced Alterations in Hepatic Perfusion and Function - Toward Multi-Scale Computational Modeling for a Better Prediction of Post-hepatectomy Liver Function.Frontiers in physiology · 2021Review
- Decellularized bovine placentome for portacavally-interposed heterotopic liver transplantation in rats.Materials science & engineering. C, Materials for biological applications · 2019Article
- The role of bile salts in liver regeneration.Hepatology international · 2016Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Portal vein ligation (PVL) induces atrophy/hypertrophy complex (AHC). We hypothesised that simultaneous bile duct and portal vein ligation (BPL) might induce proper bile acid (BA) retention to enhance AHC by activating BA-mediated FXR signalling in the intact liver and promoting apoptosis in the ligated liver. We established rat models of 90% BPL and 90% PVL and found that BPL was well-tolerated and significantly accelerated AHC. The enhanced BA retention in the intact liver promoted hepatocyte proliferation by promoting the activation of FXR signalling, while that in the ligated liver intensified caspase3-mediated apoptosis. Decreasing the BA pools in the rats that underwent BPL could compromise these effects, whereas increasing the bile acid pools of rats that underwent PVL could induce similar effects. Second-stage resection of posterior-caudate-lobe-spearing hepatectomy was performed 5 days after BPL (B-Hx), PVL (V-Hx) or sham (S-SHx), as well as whole-caudate-lobe-spearing hepatectomy 5 days after sham (S-Hx). The B-Hx group had the most favourable survival rate (93.3%, the S-SHx group 0%, the S-Hx group 26.7%, the V-Hx group 56.7%, P < 0.01) and the most sustained regeneration. We conclude that BPL is a safe and effective method, and the acceleration of AHC was bile acid-dependent.
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