cGAS-STING targeting offers therapy choice in lung diseases
Abstract Cyclic GMP/AMP (cGAMP) synthase (cGAS), along with the endoplasmic reticulum (ER)-associated stimulator of interferon genes (STING), are crucial elements of the type 1 interferon response. cGAS senses microbial DNA and self-DNA, labeling cGAS-STING as a crucial mechanism in autoimmunity, st...
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Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
Published: |
BMC
2025-02-01
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Series: | Biology Direct |
Subjects: | |
Online Access: | https://doi.org/10.1186/s13062-025-00611-4 |
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Summary: | Abstract Cyclic GMP/AMP (cGAMP) synthase (cGAS), along with the endoplasmic reticulum (ER)-associated stimulator of interferon genes (STING), are crucial elements of the type 1 interferon response. cGAS senses microbial DNA and self-DNA, labeling cGAS-STING as a crucial mechanism in autoimmunity, sterile inflammatory responses, and cellular senescence. However, chronic and aberrant activation of the cGAS-STING axis results in inflammatory and autoimmune diseases. cGAS-STING has emerged as a vital mechanism driving inflammation-related diseases, including lung diseases. Insights into the biology of the cGAS-STING pathway have enabled the discovery of small-molecule agents which have the potential to inhibit the cGAS-STING axis in lung diseases. In this review, we first outline the principal components of the cGAS-STING signaling cascade. Then, we discuss recent research that highlights general mechanisms by which cGAS-STING contributes to lung diseases. Then, we focus on summarizing a list of bioactive small-molecule compounds which inhibit the cGAS-STING pathway, reviewing their potential mechanisms.These review highlights a novel groundbreaking therapeutic possibilities through targeting cGAS-STING in lung diseases. |
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ISSN: | 1745-6150 |