ArticleAmerican journal of translational research2017
TIM-1 attenuates the protection of ischemic preconditioning for ischemia reperfusion injury in liver transplantation.
Article in American journal of translational research, 2017. 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.
- Advances in organ protection: ischemic preconditioning and erythropoietin as protective strategies.International urology and nephrology · 2025Review
- The effect of TIM1Cell death discovery · 2025Article
- The effect of TIM1Cell death & disease · 2025Article
- Immune response associated with ischemia and reperfusion injury during organ transplantation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Tim-1 Deficiency Aggravates High-Fat Diet-Induced Steatohepatitis in Mice.Frontiers in immunology · 2021Article
- Histone Methylation Inhibitor DZNep Ameliorated the Renal Ischemia-Reperfusion InjuryFrontiers in medicine · 2020Article
- Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.Cell communication and signaling : CCS · 2019Article
- Atorvastatin Induces Hepatotoxicity in Diabetic Rats via Oxidative Stress, Inflammation, and Anti-Apoptotic Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic preconditioning (IPC) has been introduced to protect grafts against ischemic reperfusion injury (IRI) during liver transplantation (LT) in recent years. However, the underlying molecular mechanisms of IPC are not fully understood. We aimed to confirm whether the efficacy of IPC is dependent on T cell Immunoglobulin and Mucin domain-containing molecules-1 (TIM-1). Quantitative real-time reverse transcription PCR and western blotting were used to detect the expression of genes of interest. Graft function was assessed using the levels of alanine transaminase (ALT) and aspartate transaminase (AST), percentage of apoptosis cells and pathological examination. IPC treatment alleviated graft function after ischemic reperfusion. AST, ALT, CD68, CD3 positive cells and tissue myeloperoxidase activity were decreased significantly by IPC. IPC decreased the expressions of the cytokines and chemokines. Compared with the IRI group, TIM-1 expression and TIM-1 positive cells were inhibited significantly in the IPC group. TIM-1 blockage abolished the protective effect of IPC on IRI damage. IPC could not further improve graft function and decrease the sequestration of immune cells after blocking TIM-1 signaling. IPC is a convenient therapeutic strategy against IRI during LT. The benefit of IPC depends on TIM-1 signaling.
Indexed as
Identifiers
28861157PMC5575180What OpenQuestion holds
Registered trials
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