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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.
Chronic Kidney Disease (CKD) is leading cause of morbidity and mortality in the elderly, yet research on aging-related CKD remains limited. As the elderly population grows, the clinical burden continues to rise, emphasizing the need for targeted interventions. Renal fibrosis is a major pathological feature of disease progression, accelerating functional decline through extracellular matrix deposition, tubular atrophy, and glomerulosclerosis. Korean Red Ginseng (KRG) is known for its anti-aging and anti-fibrotic properties, but its role in aging-related CKD is unclear. Whether KRG confers benefit specifically in the aged kidney, where repair capacity is diminished and profibrotic signaling is intensified, remains to be elucidated.
In this study, we evaluated the therapeutic potential of KRG in unilateral ureteral obstruction (UUO)-induced CKD in 8-week-old and 18-month-old mice. Aged CKD mice were orally administered KRG (50 or 200 mg/kg/day) for four weeks, while age-matched controls and CKD groups remained untreated. Renal injury was assessed using serum biochemistry, histopathology, and molecular analyses. Blood urea nitrogen (BUN) and creatinine were measured to assess renal function. H&E, PAS, and Sirius Red staining evaluated structural injury and collagen deposition and protein expression of α-smooth muscle actin (α-SMA), fibronectin, transforming growth factor-β (TGF-β), Smad3, and acyl-CoA synthetase medium-chain family member 3 (ACSM3) was analyzed by Western blotting. Transcriptomic profiling was performed to identify candidate mechanisms, and in vitro validation was performed using TGF-β–stimulated HK-2 cells.
Compared with young CKD mice, aged CKD mice exhibited aggravated renal dysfunction and fibrosis, confirming that aging exacerbates CKD progression. Histological analysis showed tubular dilation, epithelial detachment, and glomerular sclerosis, while molecular data revealed increased KIM-1, α-SMA, fibronectin, and TGF-β/Smad3 expression. KRG significantly reduced tubular and glomerular injury, collagen accumulation, and fibrosis-related markers in a dose-dependent manner. Transcriptomic profiling identified ACSM3 as a regulator that was downregulated in aged CKD but restored by KRG. Restoration of ACSM3 was accompanied by reduced H3K27 acetylation and inhibition of the TGF-β/Smad3 axis.
In vitro, TGF-β–stimulated HK-2 cells exhibited increased α-SMA, fibronectin, and Smad3, which were markedly reduced by KRG. Importantly, KRG restored ACSM3 expression and attenuated type I collagen deposition, consistent with in vivo results.
In conclusion, KRG alleviates renal fibrosis in aging-related CKD by restoring ACSM3 and modulating epigenetic and profibrotic signaling. The recovery of ACSM3, accompanied by reduced H3K27ac and TGF-β/Smad3 activation, represents a key molecular axis through which KRG exerts anti-fibrotic effects. These findings highlight ACSM3 as a novel molecular target of KRG and support its therapeutic potential for aging-related CKD.
Funding Source: This research was supported by National Research Foundation of Korea (NRF) grant funded by the Korea government (MIST)(RS-2023-00212470)
