| Literature DB >> 26577946 |
Stephen J Horgan1,2, Chris J Watson1,2, Nadia Glezeva1,2, Pat Collier1,2,3, Roisin Neary1, Isaac J Tea1, Niamh Corrigan1, Mark Ledwidge1,2, Ken McDonald1,2, John A Baugh4.
Abstract
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.Entities:
Keywords: Hypertensive heart disease; Left ventricular remodeling; Macrophages; Serum amyloid P-component; Spontaneously hypertensive rats
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Year: 2015 PMID： 26577946 DOI： 10.1007/s12265-015-9661-1
Source DB: PubMed Journal: J Cardiovasc Transl Res ISSN： 1937-5387 Impact factor: 4.132