ArticleBioscience reports2020
Fc-Elabela fusion protein attenuates lipopolysaccharide-induced kidney injury in mice.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Research trends and frontiers of the Apelin system in kidney diseases: a multi-database bibliometric analysis and cross-validation study.International urology and nephrology · 2026Review
- Context‑dependent duality of the apelin/elabela‑APJ system in diabetes and its complications (Review).International journal of molecular medicine · 2026Review
- Review
- Role and therapeutic potential of elabela in renal disease: from molecular mechanisms to clinical applications.Endocrine connections · 2025Review
- NLRP3 Inflammasome Targeting Offers a Novel Therapeutic Paradigm for Sepsis-Induced Myocardial Injury.Drug design, development and therapy · 2025Review
- The Apelin/APJ System: A Potential Therapeutic Target for Sepsis.Journal of inflammation research · 2024Review
- Prediction of cellular targets in diabetic kidney diseases with single-cell transcriptomic analysis of db/db mouse kidneys.Journal of cell communication and signaling · 2023Article
- Advances in the study of ELABELA in renal physiological functions and related diseases.Frontiers in pharmacology · 2023Review
- Effects of three types of freshIranian journal of basic medical sciences · 2023Article
- The network map of Elabela signaling pathway in physiological and pathological conditions.Journal of cell communication and signaling · 2022Article
- Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxemia-induced acute kidney injury (AKI) is a common clinical condition that lacks effective treatments. Elabela (ELA) is a recently discovered kidney peptide hormone, encoded by the gene apela, and has been reported to improve cardio-renal outcomes in sepsis. However, ELA is a small peptide and is largely unsuitable for clinical use because of its short in vivo half-life. In the present study, we evaluated the potential renoprotective effects of a long-acting constant fragment (Fc)-ELA fusion protein in liposaccharide (LPS)-induced AKI in mice. LPS administration in mice for 5 days greatly lowered the gene expression of apela and impaired kidney function, as evidenced by elevated serum creatinine and the ratio of urine protein to creatinine. In addition, renal inflammation and macrophage infiltration were apparent in LPS-challenged mice. Treatment with the Fc-ELA fusion protein partially restored apela expression and attenuated the kidney inflammation. Moreover, LPS treatment induced reactive oxygen species (ROS) production and apoptosis in kidney HK-2 cells as well as in the mouse kidney, which were mitigated by ELA or Fc-ELA treatment. Finally, we found that ELA promoted the survival of HK-2 cells treated with LPS, and this action was abolished by LY204002, a PI3K/Akt inhibitor. Collectively, we have demonstrated that the Fc-ELA fusion protein has significant renoprotective activities against LPS-induced AKI in mice.
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