The cGAS-STING pathway: The role of self-DNA sensing in inflammatory lung disease

Ruihua Ma*, Tatiana P. Ortiz Serrano, Jennifer Davis, Andrew D. Prigge, Karen M. Ridge

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

58 Scopus citations


The presence of DNA in the cytosol is usually a sign of microbial infections, which alerts the host innate immune system to mount a defense response. Cyclic GMP-AMP synthase (cGAS) is a critical cytosolic DNA sensor that elicits robust innate immune responses through the production of the second messenger, cyclic GMP-AMP (cGAMP), which binds and activates stimulator of interferon genes (STING). However, cGAS binds to DNA irrespective of DNA sequence, therefore, self-DNA leaked from the nucleus or mitochondria can also serve as a cGAS ligand to activate this pathway and trigger extensive inflammatory responses. Dysregulation of the cGAS-STING pathway is responsible for a broad array of inflammatory and autoimmune diseases. Recently, evidence has shown that self-DNA release and cGAS-STING pathway over-activation can drive lung disease, making this pathway a promising therapeutic target for inflammatory lung disease. Here, we review recent advances on the cGAS-STING pathway governing self-DNA sensing, highlighting its role in pulmonary disease.

Original languageEnglish (US)
Pages (from-to)13156-13170
Number of pages15
JournalFASEB Journal
Issue number10
StatePublished - Oct 1 2020


  • AIM2
  • DAMP
  • autoimmune disease
  • cGAMP
  • pulmonary disease

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Biochemistry
  • Biotechnology


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