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<p>The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) remains a major clinical challenge and contributes to substantial morbidity and mortality. Interleukin-4 (IL-4), a key cytokine in T helper 2 (Th2) immunity, appears to influence this trajectory in a context-dependent manner. In acute injury, IL-4 can limit inflammatory damage, support resolution, and facilitate tubular repair, in part through effects on macrophage phenotype. However, when IL-4 signaling persists during chronic injury, it may contribute to maladaptive remodeling, including activation of profibrotic myeloid and stromal programs and accumulation of extracellular matrix (ECM), thereby promoting renal fibrosis. This review summarizes evidence on IL-4’s biological properties, its canonical (Janus kinase [JAK]–signal transducer and activator of transcription 6 [STAT6]) and non-canonical (insulin receptor substrate [IRS]–phosphoinositide 3-kinase [PI3K]–protein kinase B [AKT]) signaling pathways, and its roles in renal diseases (including AKI, lupus nephritis, diabetic nephropathy, and other chronic glomerulopathies). We also evaluate the therapeutic rationale for targeting IL-4 signaling and highlight candidate molecular targets to mitigate renal fibrosis. Clarifying these determinants may help identify when and how IL-4–related pathways could be modulated to improve repair while limiting fibrosis.</p>

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The role of interleukin-4 in acute kidney injury and chronic kidney disease: a literature review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月5日

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  • Mengke Geng,
  • Yuqian Guan,
  • Keke Sun,
  • Heng Jin

摘要

The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) remains a major clinical challenge and contributes to substantial morbidity and mortality. Interleukin-4 (IL-4), a key cytokine in T helper 2 (Th2) immunity, appears to influence this trajectory in a context-dependent manner. In acute injury, IL-4 can limit inflammatory damage, support resolution, and facilitate tubular repair, in part through effects on macrophage phenotype. However, when IL-4 signaling persists during chronic injury, it may contribute to maladaptive remodeling, including activation of profibrotic myeloid and stromal programs and accumulation of extracellular matrix (ECM), thereby promoting renal fibrosis. This review summarizes evidence on IL-4’s biological properties, its canonical (Janus kinase [JAK]–signal transducer and activator of transcription 6 [STAT6]) and non-canonical (insulin receptor substrate [IRS]–phosphoinositide 3-kinase [PI3K]–protein kinase B [AKT]) signaling pathways, and its roles in renal diseases (including AKI, lupus nephritis, diabetic nephropathy, and other chronic glomerulopathies). We also evaluate the therapeutic rationale for targeting IL-4 signaling and highlight candidate molecular targets to mitigate renal fibrosis. Clarifying these determinants may help identify when and how IL-4–related pathways could be modulated to improve repair while limiting fibrosis.