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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2025-02-01
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Online Access: | https://doi.org/10.1186/s13062-025-00611-4 |
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author | Yu Wang Xuan Zhang Weixue Wang Yi Zhang Joshua S. Fleishman Hongquan Wang |
author_facet | Yu Wang Xuan Zhang Weixue Wang Yi Zhang Joshua S. Fleishman Hongquan Wang |
author_sort | Yu Wang |
collection | DOAJ |
description | 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. |
format | Article |
id | doaj-art-aa5b3bbefaaf4c2491d9f6181c1db6eb |
institution | Kabale University |
issn | 1745-6150 |
language | English |
publishDate | 2025-02-01 |
publisher | BMC |
record_format | Article |
series | Biology Direct |
spelling | doaj-art-aa5b3bbefaaf4c2491d9f6181c1db6eb2025-02-09T12:16:39ZengBMCBiology Direct1745-61502025-02-0120111810.1186/s13062-025-00611-4cGAS-STING targeting offers therapy choice in lung diseasesYu Wang0Xuan Zhang1Weixue Wang2Yi Zhang3Joshua S. Fleishman4Hongquan Wang5Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical MedicineClinical Pharmacology Research Center, Peking Union Medical College Hospital, State Key Laboratory of Complex Severe and Rare Diseases, NMPA Key Laboratory for Clinical Research and Evaluation of Drug, Beijing Key Laboratory of Clinical PK & PD Investigation for Innovative Drugs, Chinese Academy of Medical Sciences & Peking Union Medical CollegeDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical MedicineDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical MedicineDepartment of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John’s UniversityDepartment of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical MedicineAbstract 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.https://doi.org/10.1186/s13062-025-00611-4cGASSTINGAntagonistLung diseases |
spellingShingle | Yu Wang Xuan Zhang Weixue Wang Yi Zhang Joshua S. Fleishman Hongquan Wang cGAS-STING targeting offers therapy choice in lung diseases Biology Direct cGAS STING Antagonist Lung diseases |
title | cGAS-STING targeting offers therapy choice in lung diseases |
title_full | cGAS-STING targeting offers therapy choice in lung diseases |
title_fullStr | cGAS-STING targeting offers therapy choice in lung diseases |
title_full_unstemmed | cGAS-STING targeting offers therapy choice in lung diseases |
title_short | cGAS-STING targeting offers therapy choice in lung diseases |
title_sort | cgas sting targeting offers therapy choice in lung diseases |
topic | cGAS STING Antagonist Lung diseases |
url | https://doi.org/10.1186/s13062-025-00611-4 |
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