The article reviews the mechanisms and impact of sterile inflammation, which occurs in the absence of microorganisms but shares similarities with microbial-induced inflammation. Sterile inflammation is triggered by non-microbial signals, often referred to as damage-associated molecular patterns (DAMPs), which can be released during cellular injury or death. These DAMPs, such as high-mobility group box 1 (HMGB1), heat shock proteins (HSPs), uric acid, and extracellular matrix fragments, activate immune cells like neutrophils and macrophages, leading to the production of pro-inflammatory cytokines and chemokines. The review discusses the role of pattern recognition receptors (PRRs) in sensing these DAMPs, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs), and AIM2-like receptors. It also explores the mechanisms by which DAMPs activate inflammatory pathways, such as through TLRs, inflammasomes, and the interleukin-1 receptor (IL-1R). The article highlights the importance of IL-1β in sterile inflammation and its involvement in various diseases, including atherosclerosis, crystal-induced arthropathies, and type 2 diabetes. Additionally, it discusses the potential therapeutic targets for sterile inflammatory disorders, such as IL-1R blockade and TLR signaling modulation. The review emphasizes the need for further research to understand the complex interactions between DAMPs, PRRs, and inflammatory pathways in vivo.The article reviews the mechanisms and impact of sterile inflammation, which occurs in the absence of microorganisms but shares similarities with microbial-induced inflammation. Sterile inflammation is triggered by non-microbial signals, often referred to as damage-associated molecular patterns (DAMPs), which can be released during cellular injury or death. These DAMPs, such as high-mobility group box 1 (HMGB1), heat shock proteins (HSPs), uric acid, and extracellular matrix fragments, activate immune cells like neutrophils and macrophages, leading to the production of pro-inflammatory cytokines and chemokines. The review discusses the role of pattern recognition receptors (PRRs) in sensing these DAMPs, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs), and AIM2-like receptors. It also explores the mechanisms by which DAMPs activate inflammatory pathways, such as through TLRs, inflammasomes, and the interleukin-1 receptor (IL-1R). The article highlights the importance of IL-1β in sterile inflammation and its involvement in various diseases, including atherosclerosis, crystal-induced arthropathies, and type 2 diabetes. Additionally, it discusses the potential therapeutic targets for sterile inflammatory disorders, such as IL-1R blockade and TLR signaling modulation. The review emphasizes the need for further research to understand the complex interactions between DAMPs, PRRs, and inflammatory pathways in vivo.