ArticleEuropean journal of medical research2023
Complement C3 mediates podocyte injury through TLR4/NFΚB-P65 signaling during ischemia-reperfusion acute kidney injury and post-injury fibrosis.
Article in European journal of medical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Finerenone attenuates chronic fibrotic remodeling during the AKI-CKD transition in an ischemia-reperfusion-induced acute kidney injury mouse model.Renal failure · 2026Article
- Network pharmacology, single-cell transcriptomics, machine learning and experimental validation identifying CHEK2 and HPGD as key therapeutic targets of berberine in diabetic nephropathy.Functional & integrative genomics · 2026Article
- Adipose-derived mesenchymal stem cells improved acute renal failure induced by ischemia-reperfusion injury: Focusing on toll-like receptor 4 activity and endoplasmic reticulum stress response.Journal of physiology and biochemistry · 2026Article
- Immunoinflammatory biomarkers for sepsis-associated acute kidney injury: a multicenter prospective cohort study.Immunity & ageing : I & A · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Renoprotective Effects of Phloretin and TUDCA via Simultaneous Inhibition of TLR4/MyD88/NF-κB and BiP/PERK/CHOP Pathways in AKI Under Diabetic Condition.Applied biochemistry and biotechnology · 2025Article
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Single-cell analysis reveals shared adaptive responses across different types of podocyte injury.Frontiers in immunology · 2025Article
- Complement activation in wasp venom-induced acute kidney injury.Renal failure · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study was to explore the mechanism of complement C3a mediating podocyte injury during ischemia-reperfusion acute kidney injury (IR-AKI) and post-injury fibrosis.
methodsRenal artery clamping was used to establish IR-AKI and post-injury fibrosis model. HE and Masson staining were performed to observe renal fibrosis. The protein abundance levels were measured along with inflammatory markers, renal complement C3. Podocytes were treated with C3a with or without Toll-like receptor 4(TLR4) inhibitor. The effects of TLR4 up-regulation by TLR4 plasmids were examined.
resultsC3
conclusionOur results indicate that modulating C3/TLR4/NFκB-P65 signaling pathway is a novel therapeutic target for the IR-AKI and post-injury fibrosis.
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