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Low syntaxin 17 expression in donor liver is associated with poor graft prognosis in recipients of living donor liver transplantation

Aim Liver transplantation (LT) is the only curative therapy for decompensated liver cirrhosis. For recipients of living donor LT (LDLT), restoration of liver function after transplantation is highly dependent on liver regenerative capacity, which requires large amounts of intracellular energy. Mitoc...

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Published in:Hepatology research 2022-10, Vol.52 (10), p.872-881
Main Authors: Tomiyama, Takahiro, Shimokawa, Masahiro, Harada, Noboru, Toshida, Katsuya, Morinaga, Akinari, Kosai‐Fujimoto, Yukiko, Tomino, Takahiro, Kurihara, Takeshi, Nagao, Yoshihiro, Toshima, Takeo, Morita, Kazutoyo, Itoh, Shinji, Yoshizumi, Tomoharu
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Language:English
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Summary:Aim Liver transplantation (LT) is the only curative therapy for decompensated liver cirrhosis. For recipients of living donor LT (LDLT), restoration of liver function after transplantation is highly dependent on liver regenerative capacity, which requires large amounts of intracellular energy. Mitochondrial metabolism provides a stable supply of adenosine 5′‐triphosphate (ATP) for liver regeneration. Mitophagy is a selective process in which damaged, non‐functional mitochondria are degraded and replaced with new functional mitochondria. We investigated the relationship between expression of Syntaxin17 (STX17), a key protein in mitophagy regulation, in donor livers and graft survival. Methods We examined STX17 expression in grafts from 143 LDLT donors who underwent right lobe resection and investigated the relationship between STX17 expression and graft function. We investigated the correlations among STX17 expression, mitochondrial membrane potential and cell proliferation, using a STX17‐knockdown hepatocyte cell line. Results Recipients transplanted with low STX17‐expression grafts had significantly lower graft survival rates than recipients transplanted with high STX17‐expression grafts (88.9% vs. 100%, p 
ISSN:1386-6346
1872-034X
DOI:10.1111/hepr.13809