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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.
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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.
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Abstract titles should be brief and reflect the content of the abstract.
Lysyl-tRNA synthetase 1 (KARS1) is an enzyme that catalyzes the attachment of lysine to tRNA during protein synthesis. Recent studies have suggested a non-canonical role for KARS1 as a signaling molecule that activates monocytes and macrophages and regulates their migration. Although KARS1 is known to be associated with inflammation and fibrosis in liver diseases, its role in chronic kidney disease (CKD) remains unclear. CKD is characterized by persistent macrophage infiltration, chronic inflammation, and fibrosis, ultimately leading to renal dysfunction. In this context, KARS1 may mediate the inflammation–fibrosis axis in the kidney. However, this relationship has not yet been studied. This study aims to elucidate how KARS1 contributes to renal injury, particularly whether it promotes inflammation and fibrosis through macrophage activation, and whether its inhibition can alleviate these pathological processes in CKD.
To investigate the role of KARS1 in chronic renal injury, CKD was induced in mice by feeding a 0.2% adenine diet for 2 weeks. Mice were divided into three groups (n = 6/group): Control, CKD, and CKD treated with a KARS1 modulator (ZMC002, 25 mg/kg/day PO, Zymedi Korea). KARS1 expression and cell-specific localization were analyzed by immunostaining using macrophage (F4/80) and proximal tubular (Lotus tetragonolobus lectin; LTL) markers. Serum KARS1 levels were measured by ELISA. Renal function was assessed by blood urea nitrogen (BUN) and cystatin C levels. Kidney injury and fibrosis were evaluated using Masson’s Trichrome (MT) and Periodic Acid-Schiff (PAS) staining. Damaged tubular, inflammatory, macrophage, and fibrosis markers were examined by qPCR and immunostaining. Statistical analysis used one-way ANOVA followed by Tukey’s post hoc test.
KARS1 was highly expressed in F4/80⁺ macrophages and LTL–positive proximal tubular cells in CKD mice. Serum KARS1 levels were significantly elevated in the CKD group compared with the control group (p < 0.01). In the CKD group, BUN and serum cystatin C levels were significantly increased compared with the control group (p < 0.01); however, these parameters were markedly reduced in the KARS1 modulator–treated CKD group, indicating a recovery of renal function (p < 0.001). Histological analyses using PAS and MT staining revealed tubular injury and fibrosis in CKD kidneys relative to the control group, both of which were notably alleviated by KARS1 modulation (p < 0.01). Immunostaining analysis revealed that the expression of VCAM-1, a marker of damaged tubular cells, was significantly increased in CKD mice compared with the control group but was markedly reduced in KARS1 modulator–treated mice (p < 0.001). In addition, the expression of fibrosis markers (collagen I and α-SMA) and macrophage markers (CD68 and CD206) was elevated in CKD mice compared with controls but was significantly decreased following KARS1 modulation (p < 0.05). Furthermore, qPCR analysis revealed that the expression of inflammatory markers (TNF-α and iNOS) was elevated in CKD mice compared with controls but was significantly reduced following KARS1 modulation (p < 0.01).
Our results indicate, for the first time, an increased expression of KARS1 in kidney fibrosis and that KARS1 modulation could be effective by inhibiting inflammation and fibrosis in CKD.
