The findings provide the scientific foundation for Arch Biopartners’ new CKD platform, expanding the Company’s kidney therapeutics pipeline beyond acute injury to chronic disease.
Overview
The research published in JASN shows that the inflammatory protein IL-32 localizes to lipid droplets in kidney tubular cells, where it drives mitochondrial dysfunction contributing to injury in DKD. This is the first evidence that lipid droplets function as inflammatory platforms linking metabolic stress to progressive kidney damage.
In preclinical models, blocking IL-32 reduced tubular injury, while treatment with the SGLT2 inhibitor canagliflozin lowered IL-32 expression, underscoring the immediate clinical relevance of this pathway. As a human-specific cytokine, IL-32 offers a differentiated and targetable mechanism for next-generation therapies and biomarker development in DKD, the leading cause of kidney failure worldwide.
Publication Details
Citation
IL-32 Is a Lipid Droplet-Associated Mediator of Tubular Injury in Diabetic Kidney Disease: FR-PO289. Journal of the American Society of Nephrology 35(10S):10.1681/ASN.2024p4xmck6v, October 2024. | DOI: 10.1681/ASN.2024p4xmck6v
Authors
Chung, Hyunjae; Sinha, Sarthak; Chappellaz, Mona L.; Lau, Arthur; Rahmani, Waleed; Belay, Sisay G.; Swamy, Asha K. R.; Chapman, Kevin R.; Andonegui, Graciela; Benediktsson, Hallgrimur; Stys, Peter K.; Muruve, Daniel A.; Chun, Justin.
