Long noncoding RNAs (lncRNAs) play crucial roles in human inflammatory diseases by regulating gene expression and signaling pathways. This review summarizes the expression levels and regulatory mechanisms of lncRNAs in various inflammatory diseases, including cardiovascular disease, osteoarthritis, sepsis, chronic obstructive pulmonary disease, asthma, acute lung injury, diabetic retinopathy, and Parkinson's disease. LncRNAs influence inflammatory responses through mechanisms such as transcription regulation, mRNA stability, miRNA sponge activity, and signaling pathways. They also regulate macrophage polarization, which is essential for controlling inflammation. For example, lncRNA FA2H-2 and MLKL are involved in atherosclerosis, while lncRNA CCL2 promotes vascular inflammation. LncRNAs like HIF1A-AS2 and H19 modulate inflammatory responses by interacting with miRNAs. In sepsis, lncRNAs such as NKILA and TUG1 regulate inflammation and immune responses. In respiratory diseases, lncRNAs like MEG3 and SNHG5 affect inflammation and cell survival. In diabetic retinopathy, lncRNAs such as SNHG7 and HOTAIR influence inflammation and cell function. In Parkinson's disease, lncRNAs like SNHG7 and HOTAIR modulate inflammation and neurodegeneration. LncRNAs also regulate macrophage polarization, with some promoting M1 polarization and others aiding M2 polarization. Despite growing evidence of their roles, the exact mechanisms of lncRNAs in inflammatory diseases remain to be fully understood. These findings suggest that lncRNAs could serve as potential therapeutic targets for inflammatory diseases. Further research is needed to elucidate their mechanisms and explore their clinical applications.Long noncoding RNAs (lncRNAs) play crucial roles in human inflammatory diseases by regulating gene expression and signaling pathways. This review summarizes the expression levels and regulatory mechanisms of lncRNAs in various inflammatory diseases, including cardiovascular disease, osteoarthritis, sepsis, chronic obstructive pulmonary disease, asthma, acute lung injury, diabetic retinopathy, and Parkinson's disease. LncRNAs influence inflammatory responses through mechanisms such as transcription regulation, mRNA stability, miRNA sponge activity, and signaling pathways. They also regulate macrophage polarization, which is essential for controlling inflammation. For example, lncRNA FA2H-2 and MLKL are involved in atherosclerosis, while lncRNA CCL2 promotes vascular inflammation. LncRNAs like HIF1A-AS2 and H19 modulate inflammatory responses by interacting with miRNAs. In sepsis, lncRNAs such as NKILA and TUG1 regulate inflammation and immune responses. In respiratory diseases, lncRNAs like MEG3 and SNHG5 affect inflammation and cell survival. In diabetic retinopathy, lncRNAs such as SNHG7 and HOTAIR influence inflammation and cell function. In Parkinson's disease, lncRNAs like SNHG7 and HOTAIR modulate inflammation and neurodegeneration. LncRNAs also regulate macrophage polarization, with some promoting M1 polarization and others aiding M2 polarization. Despite growing evidence of their roles, the exact mechanisms of lncRNAs in inflammatory diseases remain to be fully understood. These findings suggest that lncRNAs could serve as potential therapeutic targets for inflammatory diseases. Further research is needed to elucidate their mechanisms and explore their clinical applications.