ArticleCell death discovery2024
Epithelial CEBPD activates fibronectin and enhances macrophage adhesion in renal ischemia-reperfusion injury.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Article
- Cage-Farming Causes Histopathological Alterations in the Renal Tissues of the Rainbow TroutInternational journal of molecular sciences · 2025Article
- Topography-based implants for bone regeneration: Design, biological mechanism, and therapeutics.Materials today. Bio · 2025Review
- Supervised Machine-Based Learning and Computational Analysis to Reveal Unique Molecular Signatures Associated with Wound Healing and Fibrotic Outcomes to Lens Injury.International journal of molecular sciences · 2025Article
- Transcriptomics of Various Diseases Reveals the Core Role of Immune System Pathways in Retinal Damage Repair and Nerve Regeneration.Molecular neurobiology · 2025Article
- Anti-Inflammatory Effects of Polyglycerol Sulfates and Natural Polyanions in Type 2 Inflammation.Biomacromolecules · 2025Article
- Spatial transcriptomics reveals prognostically LYZCancer immunology, immunotherapy : CII · 2025Article
- Transcriptomic profiling during normothermic machine perfusion of human kidneys reveals a pro-inflammatory cellular landscape and gene expression signature associated with severe ischemia-reperfusion injury and delayed graft function.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Ischemia-reperfusion injury (IRI) is a cause of acute kidney injury in patients after renal transplantation and leads to high morbidity and mortality. Damaged kidney resident cells release cytokines and chemokines, which rapidly recruit leukocytes. Fibronectin (FN-1) contributes to immune cell migration, adhesion and growth in inflamed tissues. CCAAT/enhancer-binding protein delta is responsive to inflammatory cytokines and stresses and plays functional roles in cell motility, extracellular matrix production and immune responses. We found that the expression of CCAAT/enhancer-binding protein delta was increased in renal epithelial cells in IRI mice compared with sham mice. Following IRI, the colocalization of FN-1 with the macrophage marker F4/80 was increased in renal injury model wild-type mice but was significantly attenuated in Cebpd-deficient mice. Inactivation of CEBPD can repress hypoxia-induced FN-1 expression in HK-2 cells. Moreover, the inactivation of CEBPD and FN-1 also reduces macrophage accumulation in HK-2 cells. These findings suggest that the involvement of CEBPD in macrophage accumulation through the activation of FN-1 expression and the inhibition of CEBPD can protect against renal IRI.
Identifiers
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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.