The CGAS-STING1 Pathway as a Mediator of Innate Immune Response in Cardiovascular Disease

Authors

Leila Rouhi
Priyatansh Gurha
Ali J Marian

Language

English

Publication Date

4-1-2025

Journal

JACC: Asia

DOI

10.1016/j.jacasi.2025.01.005

PMID

40180542

PMCID

PMC12081230

PubMedCentral® Posted Date

3-18-2025

PubMedCentral® Full Text Version

Post-print

Abstract

The innate immune response, a rapid and cell-autonomous response of the cell to the pathogens, recognizes the external as well as the internal pathogens, such as self-DNA, released from the damaged cells. The response activates a set of molecules that induce the expression of proinflammatory cytokines and chemokines and leads to inflammation, fibrosis, and cell death. The innate immune response comprised of DNA-sensing protein cyclic guanosine monophosphate-adenosine monophosphate synthase (CGAS) and its downstream molecules, the stimulator of interferon genes 1 (STING1), TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and nuclear factor kappa B (NFκB), are activated in several cardiovascular diseases, including hereditary cardiomyopathies, myocardial infarction, hypertension, atherosclerosis, and aortic aneurysm. The genetic deletion of key molecules in this pathway, such as CGAS, STING1, and interferon regulatory factor 3, affords salubrious effects, including improving survival and cardiac dysfunction, rendering the CGAS-STING1 pathway an attractive therapeutic target in cardiovascular disease.

Keywords

ardiomyopathy, CGAS, cytosolic DNA, DNA damage response, heart failure, immunity

Published Open-Access

yes

Recommended Citation

Leila Rouhi, Priyatansh Gurha, and Ali J Marian, "The CGAS-STING1 Pathway as a Mediator of Innate Immune Response in Cardiovascular Disease" (2025). Faculty, Staff and Student Publications. 5787.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/5787