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<p>The interplay between autophagy and microRNAs (miRNAs) has emerged as a pivotal regulatory axis in the pathogenesis of kidney diseases, offering novel therapeutic targets for conditions such as renal ischemia–reperfusion injury (RIRI), acute kidney injury (AKI), diabetic nephropathy (DN), and renal cell carcinoma (RCC). Autophagy, a conserved cellular process, plays a dual role in kidney homeostasis, acting as both a protective mechanism and a contributor to disease progression depending on context. Dysregulation of autophagy is implicated in renal fibrosis, tubular cell apoptosis, and podocyte injury, while miRNAs, as post-transcriptional regulators, modulate autophagy pathways to influence disease outcomes. In RIRI and AKI, miRNAs such as miR-192-5p, miR-30a-5p, and miR-92a regulate autophagy to mitigate oxidative stress and inflammation, whereas in DN, miR-214 and miR-22 disrupt autophagic flux, exacerbating fibrosis and podocyte dysfunction. In RCC, oncogenic miRNAs like miR-204 and miR-30a-3p hijack autophagy to promote tumor survival and chemoresistance. Therapeutic strategies, including miRNA mimics/inhibitors, natural compounds (e.g., curcumin, oleanolic acid), and stem cell-derived exosomes, demonstrate promise in preclinical models by restoring autophagic balance. This review highlights the intricate crosstalk between miRNAs and autophagy in kidney diseases, elucidating underlying molecular mechanisms. This article aligns with SDG 3 (Good Health and Well-Being) of the UN Agenda for Sustainable Development.</p>

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The interplay between autophagy and microRNAs in kidney diseases: possible therapeutic crosstalk for targeted therapy

  • 期刊论文

  • 发表日期：

    2026年6月23日

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  • Omer Qutaiba Baderaldeen Allela,
  • Ali Fawzi Al-Hussainy,
  • Subbulakshmi Ganesan,
  • Aditya Kashyap,
  • Krishnakumar Samikan,
  • Rajashree Panigrahi,
  • Abduhalim Muminov,
  • Sada Ghalib Taher,
  • Mariem Alwan,
  • Mahmood Jawad,
  • Hiba Mushtaq,
  • Bagher Farhood

摘要

The interplay between autophagy and microRNAs (miRNAs) has emerged as a pivotal regulatory axis in the pathogenesis of kidney diseases, offering novel therapeutic targets for conditions such as renal ischemia–reperfusion injury (RIRI), acute kidney injury (AKI), diabetic nephropathy (DN), and renal cell carcinoma (RCC). Autophagy, a conserved cellular process, plays a dual role in kidney homeostasis, acting as both a protective mechanism and a contributor to disease progression depending on context. Dysregulation of autophagy is implicated in renal fibrosis, tubular cell apoptosis, and podocyte injury, while miRNAs, as post-transcriptional regulators, modulate autophagy pathways to influence disease outcomes. In RIRI and AKI, miRNAs such as miR-192-5p, miR-30a-5p, and miR-92a regulate autophagy to mitigate oxidative stress and inflammation, whereas in DN, miR-214 and miR-22 disrupt autophagic flux, exacerbating fibrosis and podocyte dysfunction. In RCC, oncogenic miRNAs like miR-204 and miR-30a-3p hijack autophagy to promote tumor survival and chemoresistance. Therapeutic strategies, including miRNA mimics/inhibitors, natural compounds (e.g., curcumin, oleanolic acid), and stem cell-derived exosomes, demonstrate promise in preclinical models by restoring autophagic balance. This review highlights the intricate crosstalk between miRNAs and autophagy in kidney diseases, elucidating underlying molecular mechanisms. This article aligns with SDG 3 (Good Health and Well-Being) of the UN Agenda for Sustainable Development.