MiRNA-loaded MSC exosomes restore autophagy flux for acute pancreatitis therapy

Haojie Zeng1,2,3, Tonghua Wu1,2,3, Si Luo1,2,3

  • 1The First School of Clinical Medicine, Guangdong Medical University, Zhanjiang, Guangdong, China.

Frontiers in Immunology
|August 22, 2025
PubMed

Insights

Mesenchymal stem cells (MSCs) and their exosomes show promise for treating acute pancreatitis (AP) by delivering microRNAs to regulate inflammation and restore cell function. Further research is needed to optimize delivery and ensure safety for clinical application.

Area of Science:

  • Biomedical Science
  • Cell Biology
  • Regenerative Medicine

Background:

  • Acute pancreatitis (AP) is a severe condition linked to autophagy imbalance and inflammation.
  • Autophagy's role in AP is complex, acting as a double-edged sword.
  • Current treatments for AP lack targeted mechanisms for cellular repair and homeostasis.

Purpose of the Study:

  • To review the therapeutic potential of mesenchymal stem cells (MSCs) and their exosomes in treating AP.
  • To explore how MSC-derived exosomes deliver microRNAs (miRNAs) to modulate key signaling pathways.
  • To identify strategies for improving AP treatment through exosome-based therapies.

Main Methods:

  • Systematic review of existing literature on MSCs, exosomes, and miRNAs in AP.
  • Analysis of miRNA targeting of pathways like PI3K/AKT/mTOR.
  • Evaluation of exosome-mediated effects on inflammation, regeneration, and autophagy.

Main Results:

  • MSC-derived exosomes deliver functional miRNAs that can target pathways like PI3K/AKT/mTOR.
  • These miRNAs contribute to anti-inflammatory effects, promote tissue regeneration, and restore autophagy homeostasis.
  • Exosomes offer a potential strategy for modulating AP pathology.

Conclusions:

  • MSC-derived exosomes represent a promising therapeutic avenue for acute pancreatitis.
  • Further research is required to standardize exosome preparation and optimize miRNA delivery efficiency.
  • Addressing challenges in safety evaluation and understanding the intricate "cell-vesicle-miRNA-target pathway" is crucial for clinical translation.