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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.
Renal fibrosis is pathologically defined by excessive deposition of extracellular matrix (ECM) components such as collagen and fibronectin. Recent studies highlight the link between ECM mechanical properties and renal fibrosis regulation. Our study aims to explore the molecular mechanisms by which mechanical signal molecule-mediated ECM stiffness promotes renal fibrosis development.
Healthy subjects and patients with renal interstitial fibrosis were recruited, with renal matrix stiffness measured by elastic ultrasound. A unilateral ureteral obstruction (UUO) model was established in C57 wild-type mice, and intervention groups were given intraperitoneal injection of normal saline or lysyl oxidase-like 2 (LOXL2) inhibitor (BAPN, 150 mg/kg/day) after operation. Kidney samples were collected at 7 and 14 days post-UUO to evaluate pathological changes of obstructed kidneys, as well as localization, protein and mRNA abundances of LOXL2, FN, COL1A1, Plin2, CPT1A and FXR. Atomic force microscopy measured mouse kidney Young's modulus. Fibronectin-coated cell culture systems (6 kPa, 16 kPa) were established, with HK-2 and MTEC cells seeded separately. Differences in growth, viability, phenotype of the two cell types between high- and normal-stiffness media were compared, as well as changes in cell phenotype and fatty acid oxidative metabolism after LOXL2 silencing.
Elastic ultrasound has confirmed that the renal matrix stiffness of healthy subjects is significantly lower than that of patients with interstitial fibrosis (6.835±0.6361 kPa vs 9.986±0.2850 kPa, P<0.0001). Renal matrix stiffness in the sham operation group was significantly lower than that in the obstructed kidneys at 7 days post-surgery in a mice model of UUO (5.854±2.087 kPa vs 12.92±0.3818 kPa, P<0.01). LOX, LOXL1, and LOXL2 showed positive expression in both renal proximal tubules and interstitium, among which LOXL2 exhibited the most significant change with a disease progression-dependent increase. In vitro experimental results demonstrated that compared with cells cultured in normal stiffness, the expression of LOXL2 in HK-2 and MTEC cells under high-stiffness culture conditions was significantly upregulated, along with increased expression of FN and α-SMA. Intracellular fatty acid metabolism disorder occurred with down-regulation of CPT1A and FXR. Differential gene enrichment analysis revealed that the PI3K-AKT signaling pathway was significantly enriched in HK-2 cells cultured under high stiffness for 48 hours. After inhibiting LOXL2 expression both in vivo and in vitro, renal interstitial fibrosis was alleviated, the polarity of proximal tubular epithelial cells was partially restored, fatty acid oxidative metabolism disorders were corrected. Meanwhile, the down-regulated expressions of CPT1A and FXR were partially reversed.
These results suggest renal proximal tubular cells perceive extracellular matrix stiffness changes, and mechanical signal molecule LOXL2 may regulate fatty acid oxidative metabolism via the PI3K-AKT pathway to be involved in the development of renal fibrosis.
