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Circulating Mitochondrial DNA Stimulates Innate Immune Signaling Pathways to Mediate Acute Kidney Injury

Jiaye Liu1,2,3, Zhanjun Jia1,2,3, Wei Gong1,2,3

  • 1Nanjing Key Lab of Pediatrics, Children's Hospital of Nanjing Medical University, Nanjing, China.

Frontiers in Immunology
|July 12, 2021
PubMed

Insights

Damaged mitochondria release mitochondrial DNA (mtDNA), acting as danger signals that trigger inflammation and cell death in acute kidney injury (AKI). Targeting these pathways offers a potential strategy to reduce kidney damage.

Area of Science:

  • Nephrology
  • Mitochondrial Biology
  • Immunology

Background:

  • Mitochondrial dysfunction is a key factor in acute kidney injury (AKI) development and progression.
  • The exact mechanisms linking mitochondrial damage to AKI are complex and multifactorial.

Purpose of the Study:

  • To provide a comprehensive overview of recent research on mitochondrial DNA (mtDNA)-mediated renal pathological events in AKI.
  • To offer new insights into potential therapeutic strategies targeting mtDNA-related pathways for AKI treatment.

Main Methods:

  • Review of accumulating evidence on circulating mtDNA and its role in AKI progression.
  • Analysis of innate immune pathways activated by released mtDNA, including STING, TLR9, and NLRP3.
  • Examination of mtDNA's role in mediating tubular cell inflammation and apoptosis.

Main Results:

  • Mitochondrial DNA (mtDNA) released from damaged mitochondria acts as a danger-associated molecular pattern (DAMP).
  • mtDNA activates innate immune responses via STING, TLR9, NLRP3, and other adaptors, promoting renal tubular injury.
  • Circulating mtDNA and its associated pathways are significantly implicated in AKI progression.

Conclusions:

  • Regulating proteins involved in mtDNA-mediated pathways presents a promising therapeutic strategy for reducing renal tubular injury in AKI.
  • Understanding mtDNA's role in AKI pathogenesis is crucial for developing novel interventions.
Keywords:
NLRP3STINGTLR9acute kidney injurymitochondrial DNA

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