Serum Amyloid P-Component Prevents Cardiac Remodeling in Hypertensive Heart Disease

Stephen J Horgan, Chris J Watson, Nadia Glezeva, Pat Collier, Roisin Neary, Isaac J Tea, Niamh Corrigan, Mark Ledwidge, Ken McDonald, John A Baugh

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


The potential for serum amyloid P-component (SAP) to prevent cardiac remodeling and identify worsening diastolic dysfunction (DD) was investigated. The anti-fibrotic potential of SAP was tested in an animal model of hypertensive heart disease (spontaneously hypertensive rats treated with SAP [SHR - SAP] × 12 weeks). Biomarker analysis included a prospective study of 60 patients with asymptomatic progressive DD. Compared with vehicle-treated Wistar-Kyoto rats (WKY-V), the vehicle-treated SHRs (SHR-V) exhibited significant increases in left ventricular mass, perivascular collagen, cardiomyocyte size, and macrophage infiltration. SAP administration was associated with significantly lower left ventricular mass (p < 0.01), perivascular collagen (p < 0.01), and cardiomyocyte size (p < 0.01). Macrophage infiltration was significantly attenuated in the SHR-SAP group. Biomarker analysis showed significant decreases in SAP concentration over time in patients with progressive DD (p < 0.05). Our results indicate that SAP prevents cardiac remodeling by inhibiting recruitment of pro-fibrotic macrophages and that depleted SAP levels identify patients with advancing DD suggesting a role for SAP therapy.

Original languageEnglish
Pages (from-to)554-66
Number of pages13
JournalJournal of Cardiovascular Translational Research
Issue number9
Early online date17 Nov 2015
Publication statusPublished - Dec 2015


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