ReviewBiomolecules2019
Lipoprotein(a) as Orchestrator of Calcific Aortic Valve Stenosis.
Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- Unraveling the Link Between Aortic Stenosis and Atherosclerosis: What Have We Learned?Medicina (Kaunas, Lithuania) · 2025Review
- Fuelling aortic stenosis: the integral role of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3-mediated glycolysis in Lp(a)-induced valve inflammation.European heart journal open · 2025Article
- Mineral composition and ratios in aortic valves, serum, and epicardial fat among patients with aortic stenosis undergoing aortic valve replacement.Scientific reports · 2025Article
- Role of Lipoprotein (A) in aortic valve stenosis: Novel disease mechanisms and emerging pharmacotherapeutic approaches.International journal of cardiology. Heart & vasculature · 2024Review
- The functions of apolipoproteins and lipoproteins in health and disease.Molecular biomedicine · 2024Review
- Novel Therapeutic Approaches for the Management of Elevated Lipoprotein(a): From Traditional Agents to Future Treatment Options.Life (Basel, Switzerland) · 2024Review
- Lipoprotein a - Lp(a).Indian heart journal · 2024Review
- Lp(a) in the Pathogenesis of Aortic Stenosis and Approach to Therapy with Antisense Oligonucleotides or Short Interfering RNA.International journal of molecular sciences · 2023Review
- Treatment of Lp(a): Is It the Future or Are We Ready Today?Current atherosclerosis reports · 2023Review
- Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.International journal of environmental research and public health · 2023Review
- Lipoprotein(a) As a Potential Predictive Factor for Earlier Aortic Valve Replacement in Patients with Bicuspid Aortic Valve.Biomedicines · 2023Article
- Lipoprotein(a): Cardiovascular Disease, Aortic Stenosis and New Therapeutic Option.International journal of molecular sciences · 2022Review
- Lipoprotein(a) and Subclinical Vascular and Valvular Calcification on Cardiac Computed Tomography: The Atherosclerosis Risk in Communities Study.Journal of the American Heart Association · 2022Article
- Impact of Fetuin-A, Lp(a), matrix gla protein and macrophage density on calcific aortic valve disease: a clinical study.Lipids in health and disease · 2022Article
- Causal associations between disorders of lipoprotein metabolism and ten cardiovascular diseases.Frontiers in cell and developmental biology · 2022Article
- Asian Pacific Society of Cardiology Consensus Recommendations on Dyslipidaemia.European cardiology · 2021Review
- Decreased Glucagon-Like Peptide-1 Is Associated With Calcific Aortic Valve Disease: GLP-1 Suppresses the Calcification of Aortic Valve Interstitial Cells.Frontiers in cardiovascular medicine · 2021Article
- Vascular Calcification-New Insights Into Its Mechanism.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aortic valve stenosis (AVS) is the most prevalent valvular heart disease in the Western World with exponentially increased incidence with age. If left untreated, the yearly mortality rates increase up to 25%. Currently, no effective pharmacological interventions have been established to treat or prevent AVS. The only treatment modality so far is surgical or transcatheter aortic valve replacement (AVR). Lipoprotein(a) [Lp(a)] has been implicated as a pivotal player in the pathophysiology of calcification of the valves. Patients with elevated levels of Lp(a) have a higher risk of hospitalization or mortality due to the presence of AVS. Multiple studies indicated Lp(a) as a likely causal and independent risk factor for AVS. This review discusses the most important findings and mechanisms related to Lp(a) and AVS in detail. During the progression of AVS, Lp(a) enters the aortic valve tissue at damaged sites of the valves. Subsequently, autotaxin converts lysophosphatidylcholine in lysophosphatidic acid (LysoPA) which in turn acts as a ligand for the LysoPA receptor. This triggers a nuclear factor-κB cascade leading to increased transcripts of interleukin 6, bone morphogenetic protein 2, and runt-related transcription factor 2. This progresses to the actual calcification of the valves through production of alkaline phosphatase and calcium depositions. Furthermore, this review briefly mentions potentially interesting therapies that may play a role in the treatment or prevention of AVS in the near future.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.