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MSCs in acute kidney injury treatment: Modulating mitochondrial function and inhibiting pyroptosis via PGC-1α

Yanjun Wang1, Yanlin Ding2, Haiyun Dong2

  • 1Department of Geriatrics, Affiliated Hospital of Qinghai University, Xining, Qinghai, 810001, China; Research Center for High Altitude Medicine, Qinghai University, Xining, Qinghai, 810001, China; High-Altitude Medicine Key Laboratory of the Ministry of Education, Xining, Qinghai, 810001, China; Qinghai Provincial Key Laboratory for Application of High-Altitude Medicine (Qinghai-Utah Joint Key Laboratory for Plateau Medicine), Xining, Qinghai, 810001, China.

Experimental Cell Research
|May 5, 2025
PubMed
Abstract

Insights

Mesenchymal stem cells (MSCs) enhance acute kidney injury repair by improving mitochondrial function and inhibiting pyroptosis in renal tubular epithelial cells (RTECs). This therapy offers long-term protection against kidney fibrosis.

Area of Science:

  • Nephrology
  • Regenerative Medicine
  • Cell Biology

Background:

  • Acute kidney injury (AKI) remains a significant clinical challenge with limited therapeutic options.
  • Mesenchymal stem cells (MSCs) show promise for AKI treatment, but their precise mechanisms require further elucidation.
  • Mitochondrial dysfunction and pyroptosis are key pathological processes in AKI.

Purpose of the Study:

  • To investigate the therapeutic mechanisms of MSCs in AKI.
  • To determine the role of MSCs in regulating mitochondrial function and pyroptosis in renal tubular epithelial cells (RTECs).

Main Methods:

  • An in vivo ischemia/reperfusion (I/R) model of AKI was established.
  • Effects of MSC treatment on mitochondrial membrane potential, mitochondrial function, pyroptosis, and PGC-1α expression in RTECs were assessed.
  • Levels of pyroptotic markers and fibrotic indicators were quantified.

Main Results:

  • MSC treatment significantly improved mitochondrial function in RTECs.
  • This improvement was associated with upregulated PGC-1α expression, balanced mitochondrial dynamics, reduced mitochondrial ROS, and suppressed NLRP3 inflammasome activation.
  • MSC therapy reduced pyroptotic markers (e.g., IL-18) and demonstrated long-term anti-fibrotic effects.

Conclusions:

  • MSCs promote AKI repair by modulating mitochondrial function and inhibiting pyroptosis.
  • MSC therapy offers potential for both acute recovery and long-term protection against kidney fibrosis.
  • These findings provide a theoretical basis for developing MSC-based AKI treatments.
Keywords:
Acute kidney injuryChronic kidney diseaseMesenchymal stem cellsMitochondrial dynamicsPGC-1α

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