Inhibition of Interleukin-33 to Reduce Glomerular Endothelial Inflammation in Diabetic Kidney Disease

Hofherr, Alexis; Liarte Marin, Elena; Musial, Barbara; Seth, Asha; Slidel, Tim; Conway, James; Baker, David; Hansen, Pernille B.L.; Challis, Benjamin; Bartesaghi, Stefano; Bhat, Maria; Pecoits-Filho, Roberto; Tu, Xiao; Selvarajah, Viknesh; Woollard, Kevin; Heerspink, Hiddo J.L.

doi:10.1016/j.ekir.2024.03.009

Kidney International Reports

2024

DOI: 10.1016/j.ekir.2024.03.009

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Inhibition of Interleukin-33 to Reduce Glomerular Endothelial Inflammation in Diabetic Kidney Disease

Alexis Hofherr,

Elena Liarte Marin,

Barbara Musial

et al.

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Cited by 4 publications

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Partial reduction of interleukin‐33 signaling improves senescence and renal injury in diabetic nephropathy

Chen,

Gao,

Yin

et al. 2024

MedComm

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Diabetic nephropathy (DN) is a frequent and costly complication of diabetes with limited understandings of mechanisms and therapies. Emerging evidence points to the important roles of interleukin‐33 (IL‐33) in acute kidney injury, yet its contribution to DN is still unclear. We here found a ubiquitous increase of IL‐33 and its receptor (ST2) in murine models and patients with DN. Surprisingly, both IL‐33 and ST2 knockdown aggravated renal lesions in DN, while overexpression of IL‐33 also exacerbated the condition. Further population‐based analyses revealed a positive correlation of IL‐33 expression with renal dysfunction in DN patients. Individuals with high IL‐33 expression‐related polygenic risk score had a higher DN risk. These findings confirmed the harmful effects of IL‐33 on DN. Conversely, endogenous and exogenous partial reduction of IL‐33 signaling conferred renoprotective effects in vivo and in vitro. Mechanistically, IL‐33 induced senescence by regulating cell cycle factors in HK‐2 cells, and accordingly senescence led to renal cell damage through the secretion of senescence‐related secretory phenotype (SASP) including IL‐33 and prostaglandins. Together, elevated IL‐33 accelerates cellular senescence to drive DN possibly by SASP production, while a partial blockage improves renal injury and senescence. Our findings pinpoint a possible and new avenue for DN interventions.

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Partial reduction of interleukin‐33 signaling improves senescence and renal injury in diabetic nephropathy

Chen,

Gao,

Yin

et al. 2024

MedComm

View full text Add to dashboard Cite

show abstract

Diabetic Kidney Disease

Gaddy,

Elrggal,

Madariaga

et al. 2025

Disease-a-Month

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The role of IL-1 family cytokines in diabetic cardiomyopathy

Wu,

Zeng,

Geng

et al. 2025

Metabolism

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Inhibition of Interleukin-33 to Reduce Glomerular Endothelial Inflammation in Diabetic Kidney Disease

Cited by 4 publications

References 82 publications

Partial reduction of interleukin‐33 signaling improves senescence and renal injury in diabetic nephropathy

Partial reduction of interleukin‐33 signaling improves senescence and renal injury in diabetic nephropathy

Diabetic Kidney Disease

The role of IL-1 family cytokines in diabetic cardiomyopathy

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