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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Chen, Yi Lin, Liyu Rao, Siyi Tao, Xuan Cui, Jiong Wan, Jianxin |
| Abstract | Background The 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. Methods Renal 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. Results C3−/− resulted in amelioration of renal dysfunction by reducing podocyte damage and renal fibrosis. Immunoblot with renal tissue homogenates from IR-AKI mice revealed that C3−/− decreased TLR4/Nuclear Factor-κB (NFκB)-P65. Conclusion Our results indicate that modulating C3/TLR4/NFκB-P65 signaling pathway is a novel therapeutic target for the IR-AKI and post-injury fibrosis. Graphical Abstract |
| Related Links | https://eurjmedres.biomedcentral.com/counter/pdf/10.1186/s40001-023-01054-1.pdf |
| Ending Page | 14 |
| Page Count | 14 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| DOI | 10.1186/s40001-023-01054-1 |
| Journal | European Journal of Medical Research |
| Issue Number | 1 |
| Volume Number | 28 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2023-03-27 |
| Access Restriction | Open |
| Subject Keyword | Medicine Public Health Infectious Diseases Internal Medicine Surgery Oncology Biomedicine Acute kidney injury Chronic kidney disease Podocyte Complement C3 Medicine/Public Health |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine |
| Journal Impact Factor | 2.8/2023 |
| 5-Year Journal Impact Factor | 2.9/2023 |
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