ArticleFrontiers in physiology2025
Insights into the effects of apelin-13 on renal function and NHE3 activity following ischemia/reperfusion-induced acute kidney injury.
Article in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- International Union of Basic and Clinical Pharmacology. CXXI. Apelin receptor pharmacology in the human cardiovascular system and emerging clinical applications.Pharmacological reviews · 2026Review
- Review
- Quercetin Alleviates Renal Ischemia-Reperfusion Injury by Inhibiting the STING-NF-κB Inflammatory Pathway.Dose-response : a publication of International Hormesis SocietyArticle
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5 authors.
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Abstract
Introduction: Acute kidney injury (AKI) is a clinical syndrome characterized by rapid decline in renal function with varying severity. In this context, tubular function is impaired in ischemia-induced AKI. Although there are no effective therapies for AKI, many compounds have been reported to reduce kidney injury, such as apelin-13. Considering the relevance of proximal tubular cells in maintaining fluid and electrolyte homeostasis, the effects of apelin-13 on tubular injury or sodium proximal transport remain unclear. Thus, the present study aims to evaluate the effects of exogenous administration of apelin-13 in the renal ischemia/reperfusion (I/R) model, with particular focus on renal function, injury markers, and tubular proliferation. Methods: Male C57BL/6 mice were initially treated with a vehicle or high dose of apelin-13 (200 μg/kg/day) and subjected to kidney bilateral ischemia procedure for 30 min or a sham surgery. The mice were euthanized by exsanguination 2 d after the ischemic procedure. Then, the renal function was assessed through the plasma urea level and creatinine clearance. Tubular injury was evaluated by hematoxylin and eosin staining. Kidney injury molecule 1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), megalin, Ki67, and phospho ERK 1/2 (Thr202/Tyr204) were evaluated through immunohistochemical or immunoblotting experiments. Moreover, the murine proximal tubular cells (TKPTS) were treated with apelin-13 (100 nM) to evaluate the activity of the Na Results: Initial administration of apelin-13 did not improve tubular injury, creatinine clearance, or plasma urea level after renal I/R. Moreover, KIM-1 and NGAL markers were markedly increased after renal I/R and were not reduced in the apelin-13 + I/R group. Furthermore, megalin downregulation by renal I/R was not prevented by apelin-13. Interestingly, apelin-13 worsened the renal responses to tubular proliferation after renal I/R as Ki67 and phosphorylation of ERK/1/2 (Thr202/Tyr204) were sharply reduced in the apelin-13 + I/R group. Conclusion: The overall findings suggest that apelin-13 suppresses tubular proliferation and potentially impairs the adaptive response to renal I/R injury, thereby highlighting its relevance in ischemia-induced AKI.
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