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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) affects more than 10% of the global population. Persistent kidney lesions and maladaptive repair are two major features of CKD, culminating in fibrosis and tissue dysfunction. As the primary cell type of the kidney, tubular epithelial cells (TECs) are susceptible to injury and acquire a partial epithelial-to-mesenchymal transition (pEMT) during maladaptive repair. The TECs also undergo cellular senescence, characterized by permanent cell cycle arrest and a pro-inflammatory secretome known as the SASP, leading to progressive fibrosis. Recent studies have highlighted the active role of the extracellular matrix (ECM) in CKD progression by regulating cellular processes involved in fibrosis. Among the non-structural components of the matrix, matricellular proteins play a crucial role in ECM processing and communication with embedded cells. We identified Sparc-related modular calcium-binding protein 2 (SMOC2), a matricellular protein with elevated levels in CKD, as being localized in the basement membrane of TECs after kidney injury. We hypothesize that SMOC2 is released into the epithelium after injury to regulate maladaptive repair. Here, we aim to determine the role of SMOC2 in renal fibrosis and elucidate the processes it regulates in TECs to achieve maladaptive repair after kidney injury.
We collected tissue biopsies from CKD patients, Smoc2-transgenic mice with stable Smoc2 expression, and wild-type mice for protein and RNA extraction. We used murine models of unilateral ureteral obstruction, folic acid nephropathy, aristolochic acid nephropathy, and ischemia-reperfusion to assess kidney injury, maladaptive repair, senescence, fibrosis, and SMOC2 expression. We also leveraged RNA-sequencing data from kidney-injured Smoc2-transgenic mice to identify maladaptive repair processes regulated by SMOC2. In vitro, we used the human kidney epithelial cell line HK-2 and investigated the effects of recombinant human SMOC2 protein or SMOC2 ectopic expression on the maladaptive repair of TECs at the molecular level. We also used truncated SMOC2 mutants in our studies to determine the domain that mediates binding to the ECM and exerts effects in TECs.
SMOC2 protein and mRNA levels were elevated in CKD patients and all four murine models of kidney injury. In the aristolochic acid model, SMOC2 expression was concomitant with the appearance of fibrosis and tubular senescence. Smoc2-transgenic mice developed more pEMT, inflammation, and subsequent fibrosis following injury. SMOC2 treatment or ectopic expression in HK-2 cells induced physiological changes and the expression of proteins indicative of pEMT. Notably, the extracellular calcium-binding domain of SMOC2 was sufficient to induce pEMT, and a truncated mutant lacking this domain failed to activate the pEMT properties of HK-2 cells. This domain also mediated SMOC2 binding to the basement membrane and was detected in the decellularized ECM of cultured HK-2 cells.
Our research on SMOC2, pEMT, and tubular senescence in CKD provides a unique perspective on kidney repair mechanisms and highlights a previously unknown role for SMOC2 in kidney TECs after injury.
