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<p>The kidney is a highly metabolically active organ that relies on tightly regulated organelle turnover to maintain cellular homeostasis and support its energetic demands. Autophagy, once viewed primarily as a non-selective degradation mechanism, is now recognized to encompass specialized pathways — including mitophagy, lipophagy and endoplasmic reticulum-phagy — that mediate cargo-specific quality control of subcellular organelles. These selective programmes form an integrated network that couples stress- and nutrient-sensing regulators with core autophagy machinery and lysosomal capacity, generating cell-type- and context-dependent outputs across distinct nephron segments. Selective autophagy is a central determinant of renal stress adaptation, repair and disease progression. In acute kidney injury, in&#xa0;transition from acute kidney disease to chronic kidney disease and in&#xa0;diabetic kidney disease, selective autophagy preserves organelle homeostasis; however, insufficient, excessive or mistimed autophagic flux drives tubular injury, immune remodelling and fibrosis. Lysophagy, Golgiphagy and nucleophagy are emerging pathways of selective autophagy that might also contribute to the renal stress-response network. Therapeutic strategies that target selective autophagy in the kidney will require carefully timed and precise cell-specific modulation, as well as biomarker-guided patient stratification, to improve efficacy and avoid adverse effects.</p>

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Selective autophagy in kidney health and disease

  • 期刊论文

  • 发表日期：

    2026年5月11日

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  • Ying Fu,
  • Man J. Livingston,
  • Guie Dong,
  • Anqun Chen,
  • Juan Cai,
  • Zheng Dong

摘要

The kidney is a highly metabolically active organ that relies on tightly regulated organelle turnover to maintain cellular homeostasis and support its energetic demands. Autophagy, once viewed primarily as a non-selective degradation mechanism, is now recognized to encompass specialized pathways — including mitophagy, lipophagy and endoplasmic reticulum-phagy — that mediate cargo-specific quality control of subcellular organelles. These selective programmes form an integrated network that couples stress- and nutrient-sensing regulators with core autophagy machinery and lysosomal capacity, generating cell-type- and context-dependent outputs across distinct nephron segments. Selective autophagy is a central determinant of renal stress adaptation, repair and disease progression. In acute kidney injury, in transition from acute kidney disease to chronic kidney disease and in diabetic kidney disease, selective autophagy preserves organelle homeostasis; however, insufficient, excessive or mistimed autophagic flux drives tubular injury, immune remodelling and fibrosis. Lysophagy, Golgiphagy and nucleophagy are emerging pathways of selective autophagy that might also contribute to the renal stress-response network. Therapeutic strategies that target selective autophagy in the kidney will require carefully timed and precise cell-specific modulation, as well as biomarker-guided patient stratification, to improve efficacy and avoid adverse effects.