ArticlePloS one2015
Abrogation of plasminogen activator inhibitor-1-vitronectin interaction ameliorates acute kidney injury in murine endotoxemia.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Post-treatment with H12-(ADP)-liposomes after LPS challenge ameliorated coagulopathy and critical organ injury in rats.Intensive care medicine experimental · 2026Article
- Yuanhuacine modulates lipopolysaccharide-induced interleukin-6 through regulation of the JAK1/STAT3 pathway and prevents tubular damage in acute kidney injury.Experimental and therapeutic medicine · 2025Article
- CUL4B protects kidneys from acute injury by restraining p53/PAI-1 signaling.Cell death & disease · 2024Article
- Plasminogen activator inhibitor 1 is not a major causative factor for exacerbation in a mouse model of SARS-CoV-2 infection.Scientific reports · 2023Article
- PAI-1 as a critical factor in the resolution of sepsis and acute kidney injury in old age.Frontiers in cell and developmental biology · 2023Article
- Hyperoxia Reprogrammes Microvascular Endothelial Cell Response to Hypoxia in an Organ-Specific Manner.Cells · 2022Article
- Identifying of miRNA-mRNA Regulatory Networks Associated with Acute Kidney Injury by Weighted Gene Co-Expression Network Analysis.International journal of general medicine · 2022Article
- Visceral fat-specific regulation of plasminogen activator inhibitor-1 in aged septic mice.Journal of cellular physiology · 2022Article
- The Acute Phase Response Is a Prominent Renal Proteome Change in Sepsis in Mice.International journal of molecular sciences · 2019Article
- miRNA‑mRNA regulatory network analysis of mesenchymal stem cell treatment in cisplatin‑induced acute kidney injury identifies roles for miR‑210/Serpine1 and miR‑378/Fos in regulating inflammation.Molecular medicine reports · 2019Article
- PAI1 mediates fibroblast-mast cell interactions in skin fibrosis.The Journal of clinical investigation · 2018Article
- Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation.Scientific reports · 2017Article
- Deficiency of plasminogen receptor, Plg-RJournal of thrombosis and haemostasis : JTH · 2017Article
- Circulating Vitronectin Predicts Liver Injury and Mortality in Children With Sepsis: A Prospective Observational Study.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisObservational
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis-induced acute kidney injury (AKI) contributes to the high mortality and morbidity in patients. Although the pathogenesis of AKI during sepsis is poorly understood, it is well accepted that plasminogen activator inhibitor-1 (PAI-1) and vitronectin (Vn) are involved in AKI. However, the functional cooperation between PAI-1 and Vn in septic AKI has not been completely elucidated. To address this issue, mice were utilized lacking either PAI-1 (PAI-1-/-) or expressing a PAI-1-mutant (PAI-1R101A/Q123K) in which the interaction between PAI-1 and Vn is abrogated, while other functions of PAI-1 are retained. It was found that both PAI-1-/- and PAI-1R101A/Q123K mice are associated with decreased renal dysfunction, apoptosis, inflammation, and ERK activation as compared to wild-type (WT) mice after LPS challenge. Also, PAI-1-/- mice showed attenuated fibrin deposition in the kidneys. Furthermore, a lack of PAI-1 or PAI-1-Vn interaction was found to be associated with an increase in activated Protein C (aPC) in plasma. These results demonstrate that PAI-1, through its interaction with Vn, exerts multiple deleterious mechanisms to induce AKI. Therefore, targeting of the PAI-1-Vn interaction in kidney represents an appealing therapeutic strategy for the treatment of septic AKI by not only altering the fibrinolytic capacity but also regulating PC activity.
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