Publications

Detailed Information

Evaluation of endothelial cell-specific molecule-1 as a biomarker of glycocalyx damage in canine myxomatous mitral valve disease

Cited 0 time in Web of Science Cited 0 time in Scopus
Authors

Hong, Hee-Jeong; Oh, Ye-In; Park, Su-Min; An, Ju-Hyun; Kim, Tae-Hee; Chae, Hyung-Kyu; Seo, Kyoung-won; Youn, Hwa-Young

Issue Date
2022-07-05
Publisher
BMC
Citation
BMC Veterinary Research, 18(1):261
Keywords
Cardiovascular diseaseEndothelial glycocalyxESM-1Myxomatous mitral valve disease
Abstract
Background : Endothelial cell-specific molecule-1 (ESM-1) has emerged as a potential biomarker for cardiovascular disease in humans. Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs, and we hypothesized that MMVD causes chronic inflammation that increases susceptibility to endothelial glycocalyx (eGCX) damage. In this study, we measured the concentration of ESM-1 in a group of dogs with MMVD and evaluated factors affecting eGCX damage.
Results : Sixty-four dogs (control, n = 6; MMVD, n = 58) were enrolled in this study. There was no significant difference in serum ESM-1 concentrations among the MMVD stages. The serum ESM-1 concentration was significantly higher in the death group than in the alive group in MMVD dogs. (p = 0.006). In five dogs with MMVD, serum ESM-1 concentrations tended to decrease when the cardiac drug (pimobendan, furosemide, and digoxin) dose was increased.
Conclusions : In cases where MMVD progressed to decompensated heart failure with clinical symptoms and resulted in death, the concentration of serum ESM-1 increased significantly. Therefore, ESM-1 could be utilized as a new potential negative prognostic factor in patients with MMVD.
ISSN
1746-6148
Language
English
URI
https://doi.org/10.1186/s12917-022-03344-y

https://hdl.handle.net/10371/184246
DOI
https://doi.org/10.1186/s12917-022-03344-y
Files in This Item:
Appears in Collections:

Altmetrics

Item View & Download Count

  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Share