The article reviews the emerging role of mitochondria in the innate immune response. Mitochondria, which play a central role in cellular metabolism and programmed cell death, have been shown to function as signaling platforms and contribute to effector responses in the innate immune system. The authors highlight the involvement of mitochondria in antiviral immunity, antibacterial immunity, and sterile inflammation. They discuss the mechanisms by which mitochondria regulate signaling pathways, including the recruitment of pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), nucleotide oligomerization domain (NOD)-like receptors (NLRs), C-type lectin receptors (CLRs), and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). The article also explores the role of mitochondrial dynamics, reactive oxygen species (mROS), and mitochondrial-derived damage-associated molecular patterns (DAMPs) in these processes. Specific mitochondrial proteins, such as mitochondrial antiviral signaling protein (MAVS), are discussed in detail, along with their interactions with other signaling molecules and their regulation by various factors. The authors conclude by emphasizing the importance of mROS in modulating RLR signaling and the role of mitochondrial DAMPs in activating the NLRP3 inflammasome.The article reviews the emerging role of mitochondria in the innate immune response. Mitochondria, which play a central role in cellular metabolism and programmed cell death, have been shown to function as signaling platforms and contribute to effector responses in the innate immune system. The authors highlight the involvement of mitochondria in antiviral immunity, antibacterial immunity, and sterile inflammation. They discuss the mechanisms by which mitochondria regulate signaling pathways, including the recruitment of pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), nucleotide oligomerization domain (NOD)-like receptors (NLRs), C-type lectin receptors (CLRs), and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). The article also explores the role of mitochondrial dynamics, reactive oxygen species (mROS), and mitochondrial-derived damage-associated molecular patterns (DAMPs) in these processes. Specific mitochondrial proteins, such as mitochondrial antiviral signaling protein (MAVS), are discussed in detail, along with their interactions with other signaling molecules and their regulation by various factors. The authors conclude by emphasizing the importance of mROS in modulating RLR signaling and the role of mitochondrial DAMPs in activating the NLRP3 inflammasome.