Calcific aortic stenosis: omics-based target discovery and therapy development
Open accessAbstract
Calcific aortic valve disease (CAVD) resulting in aortic stenosis (AS) is the most common form of valvular heart disease, affecting 2% of those over age 65. Those who develop symptomatic severe AS have an average further lifespan of <2 years without valve replacement, and three-quarters of these patients will develop heart failure, undergo valve replacement, or die within 5 years. There are no approved pharmaceutical therapies for AS, due primarily to a limited understanding of the molecular mechanisms that direct CAVD progression in the complex haemodynamic environment. Here, advances in efforts to understand the pathogenesis of CAVD and to identify putative drug targets derived from recent multi-omics studies [including (epi)genomics, transcriptomics, proteomics, and metabolomics] of blood and valvular tissues are reviewed. The recent explosion of single-cell omics-based studies in CAVD and the pathobiological and potential drug discovery insights gained from the application of omics to this disease area are a primary focus. Lastly, the translation of knowledge gained in valvular pathobiology into clinical therapies is addressed, with a particular emphasis on treatment regimens that consider sex-specific, renal, and lipid-mediated contributors to CAVD, and ongoing Phase I/II/III trials aimed at the prevention/treatment of AS are described.
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- Premisecitation
In the TAVR era, surgical aortic valve replacement volumes have fallen sharply, with some estimates indicating a reduction of nearly 45% over the past decade.
“in the TAVR era, SAVR volumes have dropped precipitously-some estimates place this reduction at almost 45% over the past decade.188”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [188] Mehta, 2024, Age-stratified surgical aortic valve replacement for aortic stenosis, Ann Thorac Surg source
- Interpretationreasoning
The resulting shortage of diseased human tissue from surgical aortic valve replacement is becoming an obstacle to basic science research.
“The resultant scarcity of SAVR-derived diseased human tissue samples is becoming an impediment to basic science efforts”
Quote in the paperSubstantial claim - Premisereasoning
The shortage of surgical aortic valve replacement-derived diseased human tissue has led to renewed efforts to create new animal models or engineer organoids and other three-dimensional models of calcific aortic valve disease.
“has prompted renewed attempts to develop new animal models (reviewed in Sider et al. 37 and Zhu et al. 189 ) or engineer organoids and other suitable 3D models of CAVD.108,109,[190][191][192]”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Sider et al. 37
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites Zhu et al. 189
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- cites 108,109,[190][191][192]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisereasoning
Without treatment, patients with symptomatic aortic stenosis usually progress rapidly to heart failure.
“Left untreated, these patients typically progress rapidly to heart failure”
Quote in the paperSubstantial claim - Premisenone given
Low-density lipoprotein cholesterol has a clear causal role in aortic stenosis.
“A clear causal role for low-density lipoprotein choles-”
- Also stated in: § Conclusions · plain
“terol in aortic stenosis has driven extensive trials of lipid-lowering therapies including statins, proprotein convertase subtilisin/kexin type 9 inhibitors, and lipoprotein(a) inhibitors.”
Quote in the paperNot a substantial claim - Also stated in: § Conclusions · plain
- Premisenone given
Before symptoms or cardiac dysfunction appear, activation of resident valvular interstitial and endothelial cells toward a myofibrogenic lineage by combined cardiometabolic, genetic, renal, and congenital risk factors produces an intermediate disease stage characterized by sclerotic valve leaflet thickening.
“Prior to the onset of symptoms or impairment of cardiac function, initial activation of resident valvular interstitial cells and valvular endothelial cells towards a myofibrogenic lineage by a combination of cardiometabolic, genetic, renal, and congenital risk factors leads to an intermediate disease stage marked by sclerotic valve leaflet thickening.”
Quote in the paperSubstantial claim - Premisenone given
Pharmacological modulation of dipeptidyl peptidase 4 and glucagon-like peptide 1 may directly regulate valvular interstitial cell myofibrogenesis and osteogenesis.
“Notably, pharmacological modulation dipeptidyl peptidase 4 and glucagon-like peptide 1 may also directly regulate valvular interstitial cell myofibrogenesis and osteogenesis.”
Quote in the paperNot a substantial claim
- Classified as probably not a substantial claim. 4
- May combine two claims. 6
Probably not a substantial claim: may not pass S4 (based).
Premisenone givenInhibition of the renin-angiotensin system by angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors may prevent monocyte activation and/or pro-inflammatory macrophage-derived signalling.
“though inhibition of the renin-angiotensin system by angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors may prevent monocyte activation and/or pro-inflammatory macrophage-derived signalling.”
Quote in the paperNot a substantial claimMay combine two claims.
Premisenone givenDrug targets implicated in pathological valvular interstitial cell differentiation include cadherin 11 (blocked by the monoclonal antibody SYN0012) and soluble guanylate cyclase (activated by Ataciguat).
“Drug targets implicated in pathological valvular interstitial cell differentiation also include cadherin 11 (blocked by the monoclonal antibody SYN0012) and soluble guanylate cyclase (activated by Ataciguat).”
Quote in the paperNot a substantial claimMay combine two claims.
Premisenone givenIn a small fraction of patients with valvular sclerosis, roughly 2% per year, largely unknown mechanisms drive valve cell osteogenesis and cause leaflet mineralization.
“Subsequently, in a small proportion of patients with valvular sclerosis (∼2% yearly), still largely unknown mechanisms drive valve cell osteogenesis and result in leaflet mineralization”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim. May combine two claims.
Premisenone givenNovel omics-derived pharmaceutical targets that remain to be tested in clinical trials include Sortilin (driver of valvular interstitial cell myofibro/osteogenesis), major facilitator superfamily domain containing 5 [lipoprotein(a) receptor], Apolipoprotein C-III, annexin A1/A5 (extracellular vesicle cargo/tethering), amyloid precursor protein, monoamine oxidase A, and aortic valve calcification--
“Novel omics-derived pharmaceutical targets that remain to be tested in clinical trials include Sortilin (driver of valvular interstitial cell myofibro/osteogenesis), major facilitator superfamily domain containing 5 [lipoprotein(a) receptor], Apolipoprotein C-III, annexin A1/A5 (extracellular vesicle cargo/tethering), amyloid precursor protein, monoamine oxidase A, and aortic valve calcification-”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisereasoningWithin five years of developing symptomatic aortic stenosis, about 75% of patients will need aortic valve replacement or will die.
“within 5 years of developing symptomatic aortic stenosis, ∼75% will require aortic valve replacement or die”
Quote in the paperNot a substantial claimMay combine two claims.
Premisenone givenSodium-glucose cotransporter-2 inhibitors and angiotensin II receptor blockers appear to lower mortality in aortic stenosis by mitigating heart failure and normalizing blood pressure.
“Sodium-glucose cotransporter-2 inhibitors and angiotensin II receptor blockers appear to reduce mortality in aortic stenosis via mitigation of heart failure and normalization of blood pressure”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S4 (based). May combine two claims.
Premisenone givenOther therapeutics aim to directly target calcification by impairing hydroxyapatite mineral formation (inositol-based SNF472 and INS-3001) or by stabilizing common constituents of amyloidosis (Tafamidis) that may be contained in extracellular vesicles released from osteogenic valvular interstitial cells.
“Other therapeutics aim to directly target calcification by impairing hydroxyapatite mineral formation (inositol-based SNF472 and INS-3001) or by stabilizing common constituents of amyloidosis (Tafamidis) that may be contained in extracellular vesicles released from osteogenic valvular interstitial cells.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisereasoningLeaflet mineralization reduces valve opening, raises left ventricular afterload, and induces cardiac hypertrophy.
“which reduces valve opening, increases left ventricular afterload, and induces cardiac hypertrophy.”
Quote in the paperSubstantial claim
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Ataciguat is described as both nitric oxide-dependent and independent
MinorThe table calls Ataciguat a nitric oxide-dependent sGC activator, while the main text calls it nitric oxide-independent.
“Ataciguat sGC CAVS NCT02481258 Nitric oxide-dependent sGC activator; pre-clinical studies show reduced mouse aortic valve calcification”
“The AS trial is current testing the nitric oxide-independent soluble guanylate cyclase (sGC) activator Ataciguat in patients with moderate AS;”
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“40 Vesiculomics techniques have also been applied to tissue-engineered, bio-mechanically relevant, multi-layered, 3D-bioprinted, VIC-laden hydrogel valve organoids as a means of benchmarking model performance against native human tissues.”
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Roles and Regulation of Extracellular Vesicles in Cardiovascular Mineral Metabolism
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Genes that escape X chromosome inactivation modulate sex differences in valve myofibroblasts
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Artificial Intelligence Models Reveal Sex-Specific Gene Expression in Aortic Valve Calcification
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Large-scale proteomics identifies novel biomarkers and circulating risk factors for aortic stenosis
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Self-citationComparative transcriptome profiling in human bicuspid aortic valve disease using RNA sequencing
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6 Billion People Have No Access to Safe, Timely, and Affordable Cardiac Surgical Care
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AVCAPIR: A Novel Procalcific PIWI-Interacting RNA in Calcific Aortic Valve Disease
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Cellular Landscapes of Nondiseased Human Cardiac Valves From End-Stage Heart Failure–Explanted Heart
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2020 Jeffrey M. Hoeg Award Lecture
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Self-citationPalmdelphin Regulates Nuclear Resilience to Mechanical Stress in the Endothelium
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Self-citationToll-Like Receptor 3 Mediates Aortic Stenosis Through a Conserved Mechanism of Calcification
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Sex-specific cell types and molecular pathways indicate fibro-calcific aortic valve stenosis
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Self-citationGlobal burden of calcific aortic valve disease and attributable risk factors from 1990 to 2019
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Directional Endothelial Communication by Polarized Extracellular Vesicle Release
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Self-citationEffect of evogliptin on the progression of aortic valvular calcification
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Age-stratified surgical aortic valve replacement for aortic stenosis
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A Novel Ex Vivo Model of Aortic Valve Calcification. A Preliminary Report
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TLR7 Expression Is Associated with M2 Macrophage Subset in Calcific Aortic Valve Stenosis
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Coronary Artery Disease and Aortic Valve Stenosis: A Urine Proteomics Study
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A Snapshot of Cardiology in Africa
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miR-214 is Stretch-Sensitive in Aortic Valve and Inhibits Aortic Valve Calcification
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Network-guided multiomic mapping of aortic valve calcification
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Multiple Bacteria in Calcific Aortic Valve Stenosis
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Challenges and Opportunities in Valvular Heart Disease: From Molecular Mechanisms to the Community
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Valvular Prostaglandins Are Elevated in Severe Human Aortic Valve Stenosis
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The Pathophysiologic Basis and Management of Calcific Aortic Valve Stenosis
Desai, M. Y., & D, E. B. M. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2025.06.049 · Cited by 42 · see citing works
Precision cardiovascular medicine: shifting the innovation paradigm
Aikawa, M., Sonawane, A. R., Chelvanambi, S., Asano, T., Halu, A., Matamalas, J. T., Singh, S. A., Uchida, S., Aïkawa, E., Arenas, À., et al. (2025) · Frontiers in Science · doi:10.3389/fsci.2025.1474469 · Cited by 22 · see citing works
Self-citationRisk Factors for Cardiovascular and Metabolic Disease: Integrating Traditional and Novel Paradigms
Wang, Z., Chen, S., Xu, S., & Weng, J. (2025) · iNew Medicine · doi:10.1002/inm3.70000 · Cited by 22 · see citing works
Senescence-associated metabolic alterations aggravate calcific aortic valve disease
Qian, X., Xu, L., Zheng, Y., Fan, Z., Jiang, C., Liu, Y., Tong, F., Fan, P., Chen, M., Chen, Z., et al. (2026) · European Heart Journal · doi:10.1093/eurheartj/ehag191 · Cited by 8 · see citing works
Brinck, J. W., Littmann, K., Hogling, D. E., Widman, L., Caidahl, K., Eriksson, M. J., Johnson, J., Szummer, K. E., & Bäck, M. (2025) · Journal of Internal Medicine · doi:10.1111/joim.20095 · Cited by 4 · see citing works
Self-citationCook‐Calvete, A., Delgado-Marín, M., Fernandez-Rodriguez, B. M., Zaragoza, C., & Saura, M. (2025) · Biomolecules · doi:10.3390/biom15111548 · Cited by 6 · see citing works
“The disease progresses through fibrotic thickening and calcium buildup within the aortic valve, leading to clinically apparent aortic stenosis (AS) [1].”
Weiß, L., Turner, M. E., Qin, Z., Bäck, M., & Aïkawa, E. (2026) · European Heart Journal - Valvular and Structural Heart Disease · doi:10.1093/ehjvshd/xwag018 · Cited by 4 · see citing works
Self-citationComparison of Different Osteogenic Media to Induce Aortic Valve Calcification In Vitro
Evensen, D., Karlsen, T. A., Kaljusto, M., Kvitting, J. E., Stensløkken, K., Vaage, J., & Zabirnyk, A. (2025) · Journal of the Heart Valve Society · doi:10.1177/30494826251344842 · Cited by 2 · see citing works
Clift, C. L., Goudot, G., Bogut, G., Kasai, T., van Kampen, A., Pantaleão, A. N., Messas, E., Aikawa, M., Singh, S. A., Levine, R. A., et al. (2025) · Ultrasound in Medicine & Biology · doi:10.1016/j.ultrasmedbio.2025.06.026 · Cited by 2 · see citing works
Self-citationXu, H., Xu, Y., Wang, X., et al. (2025) · Journal of Inflammation Research · doi:10.2147/jir.s540540 · Cited by 2 · see citing works
“6 Previously considered passive consequences of aging, 7,8 recent studies indicate that both AS and CAVD involve active cellular processes, sharing critical pathological mechanisms including metabolic dysregulation, 9,10 immune-mediated inflammation, 11,12 and extracellular matrix (ECM) remodeling.”
Ferroptosis promotes aortic stenosis through 5-lipoxygenase
Qin, Z., Esfahani, P. H., Pawelzik, S., et al. (2026) · European Heart Journal · doi:10.1093/eurheartj/ehag397 · Cited by 2 · see citing works
Self-citationLooking ahead to an exciting year in 2025
Lüscher, T. F. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf067 · Cited by 2 · see citing works
Self-citationBone and Cardiometabolic Connection: Crosstalk between Osteoporosis and Atherosclerosis
Sarangi, K., Sampson, S., Parinandi, N. L., & Garelnabi, M. (2025) · Cell Biochemistry and Biophysics · doi:10.1007/s12013-025-01851-x · Cited by 2 · see citing works
“Calcification of the arterial wall, particularly in the intima and atherosclerotic plaques, is evident in advanced atherosclerosis associated with an increased risk of cardiovascular events [36, 37 ].”
Focus on aortic stenosis prevention and mitral regurgitation diagnosis
Crea, F. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf015 · Cited by 1 · see citing works
oxLDL-induced aortic valve inflammation and calcification: opportunities for clinical translation
Wang, Y.-J., Matter, M. A., & Matter, C. M. (2025) · Cardiovascular Research · doi:10.1093/cvr/cvaf166 · Cited by 1 · see citing works
“Decreased levels of these cholesterol transporters induced cholesterol accumulation and inflammatory responses (interleukin [IL]-1 β , IL6, and NLRP3 [nucleotide-binding domain, leucine-rich-containing family, pyrin domaincontaining-3] inflammasome activation) associated with CAVD.”
Targeting Vascular Calcification: Novel Insights into Molecular Pathways and Clinical Interventions
Chen, J., Zhang, W., Yu, M., et al. (2026) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-025-07831-w · Cited by 1 · see citing works
“…layers—such as genomics, transcriptomics, proteomics, metabolomics, and epigenomics—researchers can gain a more comprehensive understanding of the multifaceted mechanisms underlying vascular calcification and uncover its heterogeneity across diverse physiological and pathological conditions [104].”
Bergeon, J., Chassagne, F., Fanget, M., et al. (2026) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1625436 · Cited by 1 · see citing works
Self-citationContactin-2 protects against aortic valve calcification via osteogenic differentiation inhibition
Zhou, Z., Shen, R., Chen, S., Zhang, H., Chen, L., Weng, X., Lin, X., & Chai, D. (2026) · Scientific Reports · doi:10.1038/s41598-026-42767-7 · Cited by 1 · see citing works
“Several pharmacological treatments, such as statins, angiotensin-converting enzyme inhibitors, and calcification inhibitors, have been applied in patients with CAVD, but their efficacy is unsatisfactory 5,6 .”
PRMT3-Mediated Arginine Methylation Stabilizes PCSK9 to Promote Aortic Valve Calcification
Zhang, X., Hao, Y., Han, D., Jin, X., Shang, X., Zhang, L., Gan, Z., Ye, W., Wang, S., Li, X., et al. (2026) · Circulation · doi:10.1161/circulationaha.125.078830 · Cited by 1 · see citing works
“54,55 There are no effective interventions that prevent CAVD progression.”
Tan, T., Cui, H., Zhu, E., et al. (2026) · Cardiac Research · doi:10.1097/re9.0000000000000009 · Cited by 1 · see citing works
Contemporary Management of Aortic Stenosis: Timing of Intervention and Lifetime Valve Management
Cozzi, O., & Pilgrim, T. (2026) · European Journal of Clinical Investigation · doi:10.1111/eci.70245 · Cited by 1 · see citing works
A new journal for the cardiovascular community
Lüscher, T. F., & Crea, F. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf544 · Cited by 1 · see citing works
Pedicino, D., & Liuzzo, G. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf309
Integrated multi-omics analysis reveals key hub genes and mechanisms in calcific aortic stenosis
Wang, F., Liu, S., Guo, H., Yu, J., Cui, J., Cheng, Q., Aisikeer, N., Liu, F., Duan, M.-J., Xie, X., et al. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1640014
Atherothrombosis: its mechanisms and novel targets
Crea, F. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf920
The growing role of imaging in diagnosis and risk stratification
Crea, F. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf960
Turner, M. E., Nakamura, Y., Tanaka, T., Blaser, M. C., Kasai, T., Lupieri, A., Itoh, S., Ge, R., Perez, K. A., Itagawa, R., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.17.694919
Self-citationZhuo, C., Chen, L., Sun, X., Chen, T., Cai, H., & Hu, X. (2026) · Global Heart · doi:10.5334/gh.1526
Lü, P., Liu, M., Zhang, L., Fan, J., Han, G., Hou, B., Meng, Y., Wang, L., & Sun, Y. (2026) · International Journal of General Medicine · doi:10.2147/ijgm.s590621
Lončarić, A., & Batičić, L. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48050458
“Vascular calcification is a well-established predictor of coronary heart disease and also plays a central role in the pathogenesis of calcific aortic valve disease (CAVD), a progressive disorder that leads to aortic valve stenosis and substantial cardiovascular morbidity and mortality [81–84].”
A Continuum of Atrial Peristalsis Initiates the Bicuspid to Quadricuspid Valve TransitionPreprint
Wang, J., Brown, A. L., Zhao, P., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.04.722768
“Efforts to identify therapeutic targets are complicated by an incomplete understanding of how congenital valvular structures originate and interact with their biomechanical environments 3 .”
First quinquennium completed: highlights from EHJ Open 2025
Bäck, M., Banach, M., Braunschweig, F., et al. (2026) · European Heart Journal Open · doi:10.1093/ehjopen/oeag074
Self-citationŠehović, Š., Dilić, M., Džubur, A., et al. (2026) · International Journal of Cardiology · doi:10.1016/j.ijcard.2026.134562
Nogo-B attenuates vascular calcification by activating NRF2-SLC7A11 to enhance antioxidant defense
Liang, D., Zhang, W., Zhang, H., et al. (2026) · Redox Biology · doi:10.1016/j.redox.2026.104227
“It is extensively observed in conditions such as atherosclerosis [1], hypertension [2], aortic aneurysm [3], chronic kidney disease [4], and aortic valve stenosis [5].”
Emerging Role of Sodium-Glucose Cotransporter-2 Inhibitors in Aortic Stenosis
Mazur, P. K., Kopytek, M., & Natorska, J. (2026) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2026.101595
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“…on VICs because they are the principal effectors of aortic valve calcification, controlling lesion formation through matrix remodeling, inflammatory signaling, and osteogenic differentiation [56, 57]; scRNA-seq shows SIRT1 enrichment in VIC sub-populations, especially in CKD-associated CAVD valves.”
A Multiomics Review of Aortic Stenosis
Treleaven, N., Gillies, S., Zamani, P., Seguin, A.-M., Bossé, Y., Thériault, S., Whitlock, R. P., & Paré, G. (2026) · Journal of the Heart Valve Society · doi:10.1177/30494826261468625
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Reversing the pipeline: a ‘human-first’ multi-omics approach to cardiovascular discovery
Parnasa, E., Rokach, Y., Abedat, S., Amir, O., Ben‐Dov, I. Z., & Asleh, R. (2026) · Experimental & Molecular Medicine · doi:10.1038/s12276-026-01835-8
“Multi-omics approaches that integrate genomic, transcriptomic, proteomic and metabolomic data from human valve tissue have become powerful tools for studying calci fi c AS 70,71 .”
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“Prior work has shown that metabolites related to nitric oxide metabolism, lipid homeostasis, bile acid signaling, and inflammatory pathways can distinguish patients with severe aortic stenosis from controls (Blaser et al., 2025; Lupieri, 2025; van Driel et al., 2021; Zhang et al., 2025).”
Kocher, A., Osorio-Jaramillo, E., Ad, N., et al. (2026) · Medical Hypotheses · doi:10.1016/j.mehy.2026.112171
- Authors
- Blaser, M. C., Bäck, M., Lüscher, T. F., & Aikawa, E.
- Affiliations
- Brigham and Women's Hospital (US)
- Karolinska University Hospital (SE)
- University of Zurich (CH)
- Corresponding author
- Aikawa, Elena
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2024-12-04
- Volume
- 46
- Issue
- 7
- Pages
- 620-634
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- PMC
- PMC11825147
- OpenAlex
- W4405230198
- Cited by
- 45
- References
- 178
- Citations by year
- 2026: 27 · 2025: 18
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- green
- pmc.ncbi.nlm.nih.gov
- Locations
- European Heart Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Swedish Research Council
- Swedish Heart and Lung Foundation
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Valve Diseases and Treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Aortic Disease and Treatment Approaches
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- calcific aortic stenosis, calcific aortic valve disease, valvular heart disease, drug target identification, multi-omics, single-cell omics, epigenomics, transcriptomics, proteomics, metabolomics, sex differences, renal function, lipid metabolism, aortic valve replacement, clinical trials
- MeSH terms
- Aortic Valve, Aortic Valve Stenosis, Calcinosis, Humans, Genomics, Proteomics, Metabolomics, Drug Discovery
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read under definition version 3 (extract-v3) on 2026-09-28.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-28.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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