STING activation in renal and prostatic inflammation: potential therapeutic targets and immune regulation

The cyclic GMPAMP synthase (cGAS) stimulator of interferon genes (STING) pathway is a central component of innate immunity that links cytosolic DNA sensing to type I interferon and NF-κB-driven inflammatory responses. Although transient STING stimulation facilitates antimicrobial defense, tissue remodeling, and tumor immunosurveillance, sustained or maladjusted signaling facilitates chronic sterile inflammation, fibrosis, immune impairment, and carcinogenesis. Mitochondrial injury, cellular senescence, infection-related stress, and DNA damage are caused by STING in epithelial-rich organs like the kidney and prostate, which can cause inflammatory diseases and context-dependent immunomodulation in cancer. This mini-review provides an integrated view of STING activation in renal and prostate tissues, elucidating common mechanistic activators, distinct pathological outcomes, and new translational possibilities. Most recent therapeutic strategies, such as STING agonists to promote antitumor immunity and STING inhibitors to reduce maladaptive inflammation. Further insight into cell-specific and disease-stage-dependent STING regulation will be critical for developing safe and effective interventions to achieve immune homeostasis in renal and prostate pathologies.