Mitochondria as convergence hubs for innate immunity pathways

Mitochondria have emerged as a central platform for integrating innate immune signaling by actively releasing damage-associated molecular patterns (DAMPs). Under stress or infection, these mitochondria-derived molecular signals precisely regulate the activation of cGAS-STING signaling, the NLRP3 inflammasome, and mitochondrial antiviral signaling protein (MAVS)-dependent antiviral pathways, dynamically coupling cellular metabolic states with immune responses. Recent studies have revealed that mitochondria possess dual functions as bioenergetic generators and innate immune signaling hubs in host defense, inflammation regulation, and autoimmunity. Deepening our understanding of how mitochondria synergistically integrate bioenergetics, redox homeostasis, and pattern recognition mechanisms will open novel therapeutic pathways for immune diseases. A review summarizing how mitochondria act as central hubs integrating cGAS-STING, NLRP3, and MAVS pathways, and highlighting therapeutic strategies targeting mitochondrial DAMPs in immunity.