Serum amyloid A (SAA) is a major acute-phase reactant in vertebrates, with its expression increasing up to 1000-fold during inflammation. SAA consists of two main classes: acute-phase SAA (A-SAA) and constitutive SAA (C-SAA). A-SAA is a major acute-phase protein, primarily synthesized in the liver, and is highly conserved across vertebrates. It is involved in lipid metabolism, extracellular-matrix-degrading enzymes, and chemotactic recruitment of inflammatory cells. C-SAA is mainly found in humans and mice and is minimally induced during inflammation. Both A-SAA and C-SAA are regulated by cytokine signaling pathways, particularly those of interleukin-1 (IL-1) and interleukin-6 (IL-6), and can be enhanced by glucocorticoids. Transcriptional regulation of A-SAA involves several factors, including NF-κB, C/EBP, YY1, AP-2, SAF, and Sp1. A-SAA is also post-transcriptionally regulated and is involved in the pathogenesis of chronic inflammatory diseases, including amyloidosis, atherosclerosis, and rheumatoid arthritis. The SAA family includes multiple genes and proteins, with the human SAA family containing four members and the mouse SAA family containing five. These genes are clustered in the genomes of both species and are involved in various biological functions. A-SAA is primarily associated with high-density lipoprotein (HDL) and plays a role in immune cell migration and inflammation. The structure of A-SAA includes regions that may be important for its function, such as the amyloidogenic region and binding sites for other proteins. A-SAA is induced in response to inflammatory stimuli, with its expression being regulated by various cytokines, including IL-1, TNF-α, and IL-6. The expression of A-SAA is also influenced by other factors, such as glucocorticoids and insulin. The SAA family is involved in various physiological processes, including the acute-phase response, and its regulation is complex, involving multiple transcription factors and signaling pathways. The study of SAA has provided insights into the mechanisms of inflammation and the role of SAA in disease processes.Serum amyloid A (SAA) is a major acute-phase reactant in vertebrates, with its expression increasing up to 1000-fold during inflammation. SAA consists of two main classes: acute-phase SAA (A-SAA) and constitutive SAA (C-SAA). A-SAA is a major acute-phase protein, primarily synthesized in the liver, and is highly conserved across vertebrates. It is involved in lipid metabolism, extracellular-matrix-degrading enzymes, and chemotactic recruitment of inflammatory cells. C-SAA is mainly found in humans and mice and is minimally induced during inflammation. Both A-SAA and C-SAA are regulated by cytokine signaling pathways, particularly those of interleukin-1 (IL-1) and interleukin-6 (IL-6), and can be enhanced by glucocorticoids. Transcriptional regulation of A-SAA involves several factors, including NF-κB, C/EBP, YY1, AP-2, SAF, and Sp1. A-SAA is also post-transcriptionally regulated and is involved in the pathogenesis of chronic inflammatory diseases, including amyloidosis, atherosclerosis, and rheumatoid arthritis. The SAA family includes multiple genes and proteins, with the human SAA family containing four members and the mouse SAA family containing five. These genes are clustered in the genomes of both species and are involved in various biological functions. A-SAA is primarily associated with high-density lipoprotein (HDL) and plays a role in immune cell migration and inflammation. The structure of A-SAA includes regions that may be important for its function, such as the amyloidogenic region and binding sites for other proteins. A-SAA is induced in response to inflammatory stimuli, with its expression being regulated by various cytokines, including IL-1, TNF-α, and IL-6. The expression of A-SAA is also influenced by other factors, such as glucocorticoids and insulin. The SAA family is involved in various physiological processes, including the acute-phase response, and its regulation is complex, involving multiple transcription factors and signaling pathways. The study of SAA has provided insights into the mechanisms of inflammation and the role of SAA in disease processes.