ArticleFrontiers in cardiovascular medicine2022
Role of follistatin-like 1 levels and functions in calcific aortic stenosis.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Echocardiographic Alterations in Subjects with Sarcopenia and Right Heart Failure.Medical sciences (Basel, Switzerland) · 2025Article
- Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025Review
- The Association Between Sarcopenia Index and Aortic Valve Sclerosis in Coronary Artery Disease Patients: Insights from a Retrospective Cross-Sectional Analysis and Animal Models.Vascular health and risk management · 2025Article
- Identification of Diagnostic Genes of Aortic Stenosis That Progresses from Aortic Valve Sclerosis.Journal of inflammation research · 2024Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Calcific aortic valve disease (CAVD) is a progressive disease resulting in severe calcific aortic stenosis (AS), and there is increasing interest in the discovery of novel biomarkers to identify patients with potential future calcific AS at an early stage. This study aimed to determine whether follistatin-like 1 (FSTL1) is associated with calcific AS events and its exact role in aortic valve calcification. Methods: A prospective observational cohort study involving 656 patients was performed to investigate the relationship between serum FSTL1 and calcific AS incidence during a follow-up of 5 years. Furthermore, we detected FSTL1 levels in valvular interstitial cells (VICs) from calcified valves and explored the effects of FSTL1 on VIC osteogenic differentiation Results: During a median follow-up of 5 years, lower FSTL1 levels were associated with a significantly higher risk of calcific AS events (log rank test, Conclusion: Taken together, this study provides a strong rationale to consider FSTL1 as a potential therapeutic target for calcific AS.
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