ArticleFrontiers in immunology2025
A novel GCGR/GLP-1R dual-agonist TB001 ameliorates kidney fibrosis via inhibiting PERK-mediated endoplasmic reticulum stress pathway.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Chronic kidney disease (CKD) affects over one million individuals worldwide and remain a critical economic and healthcare burden. Renal fibrosis is the hallmark of CKD. Previous reports showed that GLP-1R agonists could help prevent kidney fibrosis in diabetic patients. In this study, we aimed to determine the efficacy of a novel GLP-1R and GCGR co-agonist, TB001 in the development of renal fibrosis using both Methods: Unilateral ureteral obstruction (UUO) surgery was performed on adult B6 mice to establish a mouse model of kidney fibrosis. Mice that underwent sham surgery served as the control group. UUO mice were treated with vehicle or TB001 daily post-surgery and were sacrificed at day 14. Tissue samples were collected for immunohistochemistry and kidney mRNA gene expression analysis. Mouse tubular cells (mTECs) stimulated with TGF-β were used to model kidney fibrosis Results: Compared with vehicle treatment, TB001 treatment significantly improved renal histopathology and reduced interstitial collagen deposition and macrophage infiltration in obstructed kidneys. Both Conclusion: This study demonstrated that TB001, a novel GCGR/GLP-1R co-agonist, effectively attenuates renal fibrosis in pre-clinical models, potentially through the inhibition of PERK-mediated ER stress in tubular cells.
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