Serum Amyloid P (SAP) is a highly conserved plasma glycoprotein and a member of the pentraxin family, primarily synthesized in the liver. In mice, as in humans, SAP is constitutively present at relatively stable levels and functions in innate immunity, regulation of inflammation, and modulation of amyloid formation. SAP binds to DNA, chromatin, and amyloid fibrils, helping clear cellular debris and apoptotic cells, and also plays a role in inhibiting the deposition of amyloid fibrils, which is critical in systemic amyloidosis and chronic inflammatory conditions.
In research settings, mouse SAP is used to study innate immune function, inflammatory regulation, and amyloid-related diseases. Researchers measure SAP to understand immune complex clearance, modulation of inflammation, and the role of pentraxins in disease models such as fibrosis, atherosclerosis, and systemic amyloidosis. SAP is also explored as a therapeutic target or biomarker in studies evaluating interventions that modulate inflammation or amyloid deposition.
In clinical and translational contexts, monitoring SAP in mouse models provides insight into conditions that mimic human inflammatory, fibrotic, or amyloid diseases. Stable SAP levels make it a useful baseline biomarker, while changes in specific contexts can indicate pathological progression or therapeutic response. Measuring SAP in preclinical studies aids in the development of treatments targeting amyloid disorders, chronic inflammation, or immune regulation, bridging findings from mouse models to potential human clinical applications.
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