Minimizing the risk of small-for-size syndrome after liver surgery

Heaton, Nigel; Papamichail, Michail; Pizanias, Michail; ND, Heaton

doi:10.1016/j.hbpd.2021.12.005

Cited by 7 publications

(2 citation statements)

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“…In the case of severe chronic liver injury with abnormal liver structure and significant liver fibrosis or steatosis, the capability of liver regeneration becomes overwhelming [58]. Inadequate future liver remnant (FLR) may cause small-for-size syndrome (SFSS) and result in poor or delayed graft function, prolonged intensive care stays, and even death of the recipient [59]. Therefore, a study on liver regeneration after hepatectomy is of great value.…”

Section: Discussionmentioning

confidence: 99%

Tet2-mediated macrophage activation promotes liver regeneration

Chen

Meng²,

Xu³

et al. 2023

Preprint

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Objective Macrophages are predominant immune cells that secret IL-6 and HGF to promote liver regeneration after liver resection. Ten-eleven translocation- 2 (Tet2) DNA dioxygenase regulates the secretion of pro-inflammatory factors in macrophages. In this study, we explored the role of Tet2 in macrophages and its function independent of its enzymatic activity in liver regeneration. Methods A 70% partial hepatectomy mice model was established. Enzyme-linked immunosorbent assays, quantitative reverse transcription-polymerase chain reaction, western blotting, immunofluorescences, and flow cytometry were performed to explore the infiltration and phenotypes of immune cells in mice models. Molecular dynamics simulations were carried out to study the interaction of Tet2 with Stat1. Results We found Tet2 in macrophages negatively regulates liver regeneration in the partial hepatectomy mice model. In mechanism, Tet2 interacts with Stat1 to inhibit the expressions of proinflammatory factors and suppress liver regeneration. Tet2 inhibitor BC339 attenuated the interaction of Stat1 and Tet2, enhanced Stat1 phosphorylation, and promoted hepatocyte proliferation. Notably, Tet2 also directly affected hepatocyte proliferation, independent of the IL-6-Stat3 signaling pathway. Conclusion Tet2 in macrophages negatively regulates liver regeneration via interacting with Stat1. Our results suggest that specific targeting Tet2 in macrophages promotes the recovery of liver function after hepatectomy. Keywords Macrophage, Liver regeneration, partial hepatectomy, Tet2.

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Section: Discussionmentioning

confidence: 99%

Tet2-mediated macrophage activation promotes liver regeneration

Chen

Meng²,

Xu³

et al. 2023

Preprint

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“…Все это ведет к нарастанию отека паренхимы и компрессии внутрипеченочных артерий, что усиливает ишемический компонент патогенеза. Кроме того, хирургическая травма органа усугубляется воспалительным и иммунным ответом с элементом ишемии-реперфузии, что приводит к ишемическому некрозу гепатоцитов [8].…”

Section: цельunclassified

Pathobiochemical Features of Posthepatectomy Liver Failure and Prospects for Its Metabolic Correction

Bykov,

Shevchenko,

Tsymbalyuk

et al. 2024

Innovacionnaâ medicina Kubani

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We review the current understanding of pathophysiology and pathobiochemistry of conditions following extensive resections of the liver parenchyma and describe potential ways of surgical and metabolic correction, including promising molecular targets for therapy. Reduced residual tissue volume (small-for-size syndrome), parenchymal edema due to hyperperfusion and impaired venous blood outflow, septic complications, organ ischemia-reperfusion, mitochondrial dysfunction, and oxidative stress are considered key pathogenetic factors in liver failure development following extensive resections of the liver parenchyma. Given the above, promising ways of managing posthepatectomy conditions are the use of agents reducing portal pressure (octreotide [somatostatin analogue], terlipressin [vasopressin analogue], and propranolol), energotropic metabolic drugs (combined preparations of succinate and antioxidants, gasotransmitter donors), and antibiotics and synbiotics for prevention of infectious complications. The approaches currently used in clinical practice cannot always effectively manage complications following extensive hepatectomy, so fundamental research should focus on searching and creating effective strategies for prevention and therapy of posthepatectomy liver failure.

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