The Relationship of Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase-Stimulator of the Interferon Gene Pathway With Other Immunity Signaling Pathways in Apoptosis

Abstract

Natural immunity, the first defensive mechanism of the body against pathogen invasion, relies on nucleic acid recognition systems to detect the presence of pathogens. The cyclic GMP–AMP synthase-stimulator of interferon (IFN) gene (cGAS-STING) signaling pathway is a crucial pattern recognition and effector pathway in the innate immune system. Its primary function is to detect DNA molecules in the cytoplasm and initiate downstream signaling pathways, resulting in the production of type I IFNs and other inflammatory factors. STING, a pivotal transmembrane protein in the innate immune system, plays a vital role in the host’s ability to resist invasion by foreign pathogens. An increasing amount of evidence suggests that the cGAS-STING pathway induces apoptosis in addition to stimulating inflammatory responses and producing type I IFN. Many previous studies have so far focused on investigating the mechanisms of apoptosis induced by the cGAS-STING pathway as well as the effects that ensue. The relationship between the cGAS-STING pathway and apoptosis has been extensively examined in this article. Through endoplasmic reticulum stress, nucleotide oligomerization domain-like receptor protein-3, nuclear factor-κB (NF-κB), IFN regulatory factor 3, and IFN signals, the cGAS-STING pathway may cause apoptosis. Conversely, apoptosis could affect how the cGAS-STING pathway is regulated. It may release mitochondrial DNA to boost the process or activate caspases to suppress it. The cGAS-STING pathway plays a critical role in controlling innate immune responses, fighting off infections, and stopping the growth of tumors by stopping apoptosis.