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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Aging increases susceptibility to acute kidney injury (AKI) and worsens recovery, accelerates progression to chronic kidney disease (CKD) through maladaptive repair and fibrosis. However, the specific aging-related factors contributing to this transition remain underexplored. Apelin (APLN) signaling is a critical modulator of cardiovascular and renal physiology, known to exert anti-inflammatory and anti-fibrotic effects. This study investigated whether age-related suppression of apelinergic signaling aggravates post-ischemic fibrosis and whether APLN therapy alleviates injury and fibrotic remodeling in aged mice.
AKI was induced in 8-week-old (8wk) and 19-month-old (19m) male C57BL/6 mice using a bilateral renal artery ischemia-reperfusion (IR, 40 min) model. Tissues and serum were collected two weeks after for functional and histological evaluation. Recombinant APLN was administered intraperitoneally for two weeks prior to ischemia in 19m mice to assess APLN’s therapeutic effects on injury and fibrosis. Renal function and fibrosis were assessed using kidney function markers (blood urea nitrogen [BUN], serum creatinine [SCr]), histological analysis (H&E, PAS, Sirius Red staining), Western blotting for key proteins (KIM-1, APLN, APLNR, Smad2/3, a-SMA, E-cadherin), and RNA Microarray for transcriptomic profiling of Apln/Apela expression.
The 19m-AKI group exhibited more severe renal dysfunction (elevated BUN and SCr), tubular damage, and fibrosis compared with 8wk-AKI mice. Expression of KIM-1, α-SMA, and Smad2/3 was significantly increased, while E-cadherin decreased, indicating enhanced epithelial-to-mesenchymal transition (EMT). Transcriptomic and Western blot analyses revealed age-dependent downregulation of APLN and APLNR, with further reduction after AKI. Exogenous APLN administration in 19m-AKI mice significantly improved renal function, reduced KIM-1 levels, attenuated tubular injury and fibrosis, restored E-cadherin and APLNR expression, and suppressed Smad2/3 / α-SMA pathway.
Our findings demonstrate that age-related suppression of APLN signaling aggravates susceptibility to AKI fibrotic remodeling, contributing to CKD progression. Restoration of APLN levels in aged mice attenuated injury-induced fibrosis and preserved renal function, primarily through inhibition of the Smad2/3-α-SMA pathway and EMT. These results support the potential of APLN as a therapeutic agent for age-related kidney injury and highlight the need for further investigation into its long-term efficacy and translational potential.
This research was supported by National Research Foundation of Korea (NRF) grant funded by the Korea government (MIST) (RS-2023-00212470)
