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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.
Small proteins or micropeptides play an important role in disease pathogenesis, cell signaling and metabolic regulation.
Our previous work has shown that the micropeptide LSMEM1 shows elevated expression in various chronic kidney diseases.
We aim to elucidate the role of LSMEM1 in renal disease and to dissect the mechanisms through which its unique features as a small protein contribute to disease modulation.
LSMEM1 expression/localization was analyzed in CKD patients by IHC/IF.
Computer analysis and scRNA-seq were used to identify the structure of LSMEM1 and associated DEGs and biological processes.
The expression of LSMEM1 was assessed by in vitro and in vivo assays.
LSMEM1 gene knockout mice were generated to investigate the role of LSMEM1 in the development of renal fibrosis in CKD.
Through analysis of the NIH public database we found that LSMEM1 expression was primarily localized to the renal cortex of the kidney and LSMEM1 mRNA levels were significantly higher in CKD patients.
LSMEM1expression levels were significantly higher in CKD patients and mice (including db/db mice, STZ-induced mice, UUO mice and FA mice) compared to normal controls as detected by RT-qPCR, WB, and immunohistochemical staining.
The expression levels of LSMEM1 were positively correlated with key renal function indicators, including Scr, BUN, and UACR.
Through multiplex immunofluorescence labeling, we confirmed that LSMEM1 is primarily localized in proximal tubule cells and podocytes.
Our data localizing LSMEM1 in tubular epithelial cells and podocytes prompted scRNA-seq analysis.
This revealed a significant enrichment of lipid metabolism pathways within the tubular cell population, with the top two enriched pathways being PPAR signaling and peroxisome function. In line with this, independent datasets from other studies further support the predominant enrichment of LSMEM1 in OBN nephropathy.
We measured lipid metabolism related indexes in the serum and kidney of mice, and the results showed that after Lsmem1 knock-out, the levels of the serum and kidney triglycerides, cholesterol, and low-density lipoprotein were increased, while the high-density lipoprotein level was decreased.
Through Venn diagram analysis of differentially expressed genes associated with PPAR signaling pathway and peroxisome-related pathways, we identified solute carrier family 27 member 2 (SLC27A2/FATP2) as a candidate gene.
We also used adeno-associated virus (AAV) overexpressing LSMEM1 to inject into db/db mice.
In vitro, we constructed the lentivirus that including LSMEM1-sliencing and LSMEM1-overexpression to infect podocytes and renal proximal tube cells.
Our findings identify micropeptide LSMEM1 as a key regulator of renal lipid metabolism. It protects against CKD progression by modulating the PPAR signaling pathway and SLC27A2, highlighting its therapeutic potential.
