Modulating inflammation with interleukin 37 treatment ameliorates murine Autosomal Dominant Polycystic Kidney Disease

Zylberberg, Allara K.; Cottle, Denny L.; Runting, Jessica; Rodrigues, Grace; Tham, Ming Shen; Jones, Lynelle K.; Cumming, Helen E.; Short, Kieran M.; Zaph, Colby; Smyth, Ian M.

doi:10.1016/j.kint.2023.12.006

Kidney International

2024

DOI: 10.1016/j.kint.2023.12.006

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Modulating inflammation with interleukin 37 treatment ameliorates murine Autosomal Dominant Polycystic Kidney Disease

Allara K. Zylberberg,

Denny L. Cottle,

Jessica Runting

et al.

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2024

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Cited by 4 publications

References 69 publications

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Interleukin-37: a new therapeutic target in autosomal dominant polycystic kidney disease

Yang,

Crowley

2024

Kidney International

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Interleukin-37: a new therapeutic target in autosomal dominant polycystic kidney disease

Yang,

Crowley

2024

Kidney International

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Deciphering interleukin 37's therapeutic potential: insights into alleviating inflammation in autosomal dominant polycystic kidney disease

Xue,

Zhou,

Sun

et al. 2024

Kidney International

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STING Promotes the Progression of ADPKD by Regulating Mitochondrial Function, Inflammation, Fibrosis, and Apoptosis

Wu,

Cheng,

Lee

et al. 2024

Biomolecules

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Autosomal dominant polycystic kidney disease (ADPKD) is a predominant genetic disease, which is caused by mutations in PKD genes and is associated with DNA damage in cystic cells. The intrinsic stimulator of interferon genes (STING) pathway is crucial for recognizing damaged DNA in the cytosol, triggering the expression of inflammatory cytokines to activate defense mechanisms. However, the precise roles and mechanisms of STING in ADPKD remain elusive. In this study, we show that Pkd1 mutant mouse kidneys show upregulation of STING, which is stimulated by the DNAs of nuclear and mitochondrial origin. The activation of STING promotes cyst growth through increasing (1) the activation of NF-κB in Pkd1 mutant cells and (2) the recruitment of macrophages in the interstitial and peri-cystic regions in Pkd1 mutant mouse kidneys via NF-κB mediating the upregulation of TNF-α and MCP-1. Targeting STING with its specific inhibitor C-176 delays cyst growth in an early-stage aggressive Pkd1 conditional knockout mouse model and a milder long-lasting Pkd1 mutant mouse model. Targeting STING normalizes mitochondrial structure and function, decreases the formation of micronuclei, induces Pkd1 mutant renal epithelial cell death via p53 signaling, and decreases renal fibrosis in Pkd1 mutant mouse kidneys. These results support that STING is a novel therapeutic target for ADPKD treatment.

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Modulating inflammation with interleukin 37 treatment ameliorates murine Autosomal Dominant Polycystic Kidney Disease

Cited by 4 publications

References 69 publications

Interleukin-37: a new therapeutic target in autosomal dominant polycystic kidney disease

Interleukin-37: a new therapeutic target in autosomal dominant polycystic kidney disease

Deciphering interleukin 37's therapeutic potential: insights into alleviating inflammation in autosomal dominant polycystic kidney disease

STING Promotes the Progression of ADPKD by Regulating Mitochondrial Function, Inflammation, Fibrosis, and Apoptosis

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