ArticlePloS one2017
Does necroptosis have a crucial role in hepatic ischemia-reperfusion injury?
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Resident alveolar macrophages are highly susceptible to the induction of RIPK1/RIPK3-mediated necroptosis which promote efficient pulmonary immune response.Cell death & disease · 2025Article
- Green tea's secret weapon: a review on the protective effects of epigallocatechin-3-gallate against ischemia/reperfusion damage.Pharmacological reports : PR · 2025Review
- Review
- Exploring cell death mechanisms in liver transplantation: implications for graft survival.Frontiers in immunology · 2025Review
- Cell Death in Liver Disease and Liver Surgery.Biomedicines · 2024Review
- Article
- RIPK3 promoter hypermethylation in hepatocytes protects from bile acid-induced inflammation and necroptosis.Cell death & disease · 2023Article
- MLKL deficiency attenuated hepatocyte oxidative DNA damage by activating mitophagy to suppress macrophage cGAS-STING signaling during liver ischemia and reperfusion injury.Cell death discovery · 2023Article
- Responses of hepatic sinusoidal cells to liver ischemia-reperfusion injury.Frontiers in cell and developmental biology · 2023Review
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Liver ischaemia-reperfusion injury: a new understanding of the role of innate immunity.Nature reviews. Gastroenterology & hepatology · 2022Review
- Role of Mitochondrial Pathways in Cell Apoptosis during He-Patic Ischemia/Reperfusion Injury.International journal of molecular sciences · 2022Review
- Near-infrared fluorescence imaging with indocyanine green for assessment of donor livers in a rat model of ischemia-reperfusion.BMC gastroenterology · 2022Article
- Liver Ischemia and Reperfusion Induce Periportal Expression of Necroptosis Executor pMLKL Which Is Associated With Early Allograft Dysfunction After Transplantation.Frontiers in immunology · 2022Article
- Necroptosis in Hepatosteatotic Ischaemia-Reperfusion Injury.International journal of molecular sciences · 2020Review
- Adding the oxygen carrier M101 to a cold-storage solution could be an alternative to HOPE for liver graft preservation.JHEP reports : innovation in hepatology · 2020Article
- Aging aggravated liver ischemia and reperfusion injury by promoting hepatocyte necroptosis in an endoplasmic reticulum stress-dependent manner.Annals of translational medicine · 2020Article
- Sevoflurane Postconditioning Reduces Hypoxia-Reoxygenation Injury in H9C2 Embryonic Rat Cardiomyocytes and Targets the STRADA Gene by Upregulating microRNA-107.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Necroptosis in Cholangiocarcinoma.Cells · 2020Review
- Necroptosis in the Pathophysiology of Disease.The American journal of pathology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies have demonstrated protective effects of anti-receptor interacting protein kinase 1 (RIP1), a key necroptosis molecule. However, it is uncertain whether necroptosis has a crucial role in hepatic IR injury. Therefore, we evaluated the role of necroptosis in hepatic IR injury.
methodThe IR mice underwent 70% segmental IR injury induced by the clamping of the hepatic artery and portal vein for 1 hr followed by reperfusion for 4 hr. The key necroptosis molecules (RIP1, RIP3, and MLKL) and other key molecules of regulated necrosis (PGAM5 and caspase-1) were evaluated in the warm IR injury model. A RIP1 inhibitor (necrostain-1s) and/or an anti-mitochondrial permeability transition (MPT)-mediated necrosis mediator (cyclosporine A, CyA) were administered before clamping. Necrotic injury was quantified using Suzuki's scoring system. qRT-PCR and western blot were performed to evaluate RIP1, RIP3, MLKL and PGAM5 expressions.
resultsRIP1, RIP3, MLKL and PGAM5 expression did not change in the hepatic IR injury model. Moreover, Nec1s pretreatment did not improve histology or biochemical markers. The overall Suzuki score (cytoplasmic vacuolization, sinusoidal congestion and hepatocytes necrosis) was increased in the RIP3(-/-) mice compared to the IR group (3.5 vs. 5, p = 0.026). CyA pretreatment and/or RIP3(-/-) mice decreased Bax/Bcl2 expression; however, it did lead to an overall change in the levels of AST, ALT and LDH or necrotic injury. The Bax/Bcl2 ratio and the expression of caspase-1 and caspase-3 did not increase in our hepatic IR injury model.
conclusionKey necroptosis molecules did not increase in the necrosis-dominant hepatic IR injury model. Anti-necroptosis and/or cyclosporine-A treatment did not have an overall protective effect on necrosis-dominant hepatic IR injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.