ArticleInflammation2026
TM9SF1 Aggravates Liver Ischemia-Reperfusion Injury by Promoting Autophagy.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
Funding
Abstract
Liver transplantation (LT) remains the only effective treatment for end-stage liver disease. Autophagy critically regulates liver ischemia–reperfusion (I/R) injury. Transmembrane 9 superfamily member 1 (TM9SF1) is a transmembrane protein associated with the elevation of autophagy. However, the role and mechanism of this protein in liver I/R injury have not been explored. We observed upregulated TM9SF1 expression in liver I/R mice models and AML12 cells subjected to hypoxia-reoxygenation (H/R). Using TM9SF1 adeno-associated virus (AAV) to generate overexpression and knockdown (KD) mice with liver I/R injury, we found that TM9SF1-overexpressing mice exhibited exacerbated liver damage, inflammation, and autophagy, whereas KD-TM9SF1 mice showed opposite results. Mechanistically, we found that TM9SF1 and Annexin A2 (ANXA2) interacted and jointly promoted the expression of autophagy levels during liver I/R injury. Virtual screening of FDA-approved compounds identified lomitapide as an inhibitor that selectively suppresses TM9SF1 expression, thereby attenuating I/R injury. In general, our findings indicated that TM9SF1 and ANXA2 interact with each other, promoting autophagy levels through activating the mitogen-activated protein kinase (MAPK) pathway, thereby aggravating liver I/R injury. Targeting TM9SF1-ANXA2 may be a potential therapeutic strategy.
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