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Published on: May 10, 2021
Differential expression of GLP1R, PCSK9, and SGLT2 in human aortic versus mitral valve tissues: exploratory findings
Shou-Quan Cheng1,2, Shuo Fu1, Nai-Feng Liu2
1Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
Insights
Glucagon-like peptide-1 receptor (GLP1R), PCSK9, and SGLT2 are more expressed in aortic valves than mitral valves. While expression trends higher in calcific aortic valve disease (CAVD) tissues, this study did not confirm CAVD-specific upregulation.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Valvular Heart Disease Research
Background:
- Calcific aortic valve disease (CAVD) is a prevalent condition lacking effective pharmacological treatments.
- Understanding the molecular underpinnings of CAVD is crucial for developing new therapeutic strategies.
- This study investigates the expression of key receptors and proteins in human heart valve tissues.
Purpose of the Study:
- To compare the expression of glucagon-like peptide-1 receptor (GLP1R), PCSK9, and SGLT2 in human aortic valve (AV) and mitral valve (MV) tissues.
- To explore the potential pathophysiological relevance of these targets in the context of valvular heart disease.
- To analyze expression differences in calcified versus non-calcified AV tissues and in bicuspid aortic valve (BAV) subsets.
Main Methods:
- Human AV (n=10) and MV (n=13) tissue specimens were collected from patients undergoing valve replacement surgery.
- Immunohistochemistry (IHC) was used to assess target protein expression.
- Von Kossa staining confirmed valvular calcification, with subgroup analyses performed on calcified/non-calcified AV tissues and BAV subsets.
Main Results:
- Expression of GLP1R, PCSK9, and SGLT2 was significantly higher in AV tissues compared to MV tissues (P < 0.001).
- Expression trends for these targets were higher in calcified AV specimens than non-calcified ones, but without statistical significance (P > 0.05).
- In the BAV subgroup, calcified tissues showed significantly higher expression of all three targets compared to non-calcified tissues (P < 0.05).
Conclusions:
- The study demonstrates differential expression of GLP1R, PCSK9, and SGLT2 between human aortic and mitral valves.
- While expression trends suggest a link with calcification, particularly in BAV, these findings do not establish CAVD-specific upregulation.
- Further research is needed to elucidate the precise role of these targets in the pathogenesis of calcific aortic valve disease.
Background:
Calcific aortic valve disease (CAVD) is a common valvular heart disorder for which effective pharmacological treatments remain lacking. This study aimed to compare the expression and potential pathophysiological relevance of glucagon-like peptide-1 receptor (GLP1R), proprotein convertase subtilisin/kexin type 9 (PCSK9), and sodium-glucose cotransporter 2 (SGLT2) in human aortic valve (AV) and mitral valve (MV) tissues from patients undergoing valve replacement surgery.
Methods:
Surgically resected AV (n = 10) and MV (n = 13) tissue specimens were collected between March 2020 and December 2022. Target protein expression was assessed via immunohistochemistry (IHC), and valvular calcification was confirmed by Von Kossa staining. Subgroup analyses were performed within calcified vs. non-calcified AV tissues and within a bicuspid aortic valve (BAV) subset (n = 3 per group).
Results:
GLP1R, PCSK9, and SGLT2 expression levels were significantly elevated in AV tissues compared to MV tissues (all P < 0.001). Within calcified AV specimens, expression trends were higher than in non-calcified AV tissues, though these differences did not reach statistical difference (all P > 0.05). In the exploratory BAV subgroup (n = 3 per group), expression of all three targets was higher in calcified vs. non-calcified tissues (all P < 0.05).
Conclusion:
These findings reflect differential expression between anatomically distinct valve types and do not establish CAVD-specific upregulation.
Related Concept Videos
Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Aortic Regurgitation I: Introduction
Mitral Valve Prolapse I: Introduction

