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September 5, 2026AutoimmunityOpen Access

The m6A reader IGF2BP2 promotes proinflammatory signaling in Lupus nephritis by recognizing STAT1 m6A modifications

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Authors

CZChangZhi ZhengXXXianMei XuDWDi Wu

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Overview

Preclinical investigation reveals that IGF2BP2 exacerbates renal inflammation in lupus nephritis mouse and cell models, highlighting the IGF2BP2-STAT1 axis as a therapeutic target.

Key Points

  • To determine the role and underlying molecular mechanism of the m6A reader IGF2BP2 in renal inflammation during lupus nephritis.
  • Measured IGF2BP2 expression levels in kidney tissue samples obtained from lupus nephritis patients and MRL/lpr mice.
  • Treated MRL/lpr mice with adeno-associated virus-delivered short hairpin RNA targeting IGF2BP2 and assessed renal histology, proteinuria, and kidney function.
  • Evaluated lipopolysaccharide-stimulated human kidney tubular epithelial cells (HK-2) using RNA immunoprecipitation and luciferase reporter assays to probe IGF2BP2 and STAT1 interactions.
  • IGF2BP2 expression was significantly upregulated in renal tissues from lupus nephritis patients and mice, correlating positively with proinflammatory factor expression.
  • Knockdown of IGF2BP2 significantly ameliorated kidney injury and suppressed renal inflammation in MRL/lpr mice while blunting lipopolysaccharide-induced inflammatory signaling in HK-2 cells.
  • IGF2BP2 recognized m6A marks on STAT1 mRNA to increase its transcript stability, thereby activating downstream proinflammatory cascades that drive renal pathology.

Cite This Study

Zheng et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4126b95aff0620eb69fhttps://doi.org/10.1080/08916934.2026.2724058
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