ArticleJACC. Basic to translational science2020
Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload.
Article in JACC. Basic to translational science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Comparative Cardioprotective Effectiveness: NOACs vs. Nattokinase-Bridging Basic Research to Clinical Findings.Biomolecules · 2024Review
- Article
- Lysyl oxidase-like 2 processing by factor Xa modulates its activity and substrate preference.Communications biology · 2023Article
- Review
- The Therapeutic Potential of Anticoagulation in Organ Fibrosis.Frontiers in medicine · 2022Review
- Article
- Factor Xa Inhibition with Apixaban Does Not Influence Cardiac Remodelling in Rats with Heart Failure After Myocardial Infarction.Cardiovascular drugs and therapy · 2021Article
- The Potential Role of Coagulation Factor Xa in the Pathophysiology of COVID-19: A Role for Anticoagulants as Multimodal Therapeutic Agents.TH open : companion journal to thrombosis and haemostasis · 2020Review
- Blockade of PAR-1 Signaling Attenuates Cardiac Hypertrophy and Fibrosis in Renin-Overexpressing Hypertensive Mice.Journal of the American Heart Association · 2020Article
- Factor Xa Inhibition, A New Strategy for Prevention of Adverse Cardiac Remodeling in Early Stages?JACC. Basic to translational science · 2020Article
- Rivaroxaban improves vascular response in LPS-induced acute inflammation in experimental models.PloS one · 2020Article
Corrections and comments
- Correction · 2020-09-28Error in Image · Updated to Retraction · · see also: https://pubpeer.com/publications/8563C9AA9D17B3EEACD68159F7A988
- Retraction · 2022-09-26Concerns/Issues about Data · Duplication of/in Image · Investigation by Company/Institution · Investigation by Journal/Publisher · Manipulation of Images · Objections by Third Party · Original Data and/or Images not Provided and/or not Available · Upgrade/Update of Prior Notice(s) · · see also: https://pubpeer.com/publications/8563C9AA9D17B3EEACD68159F7A988
- Commented on by
- Erratum issuedCorrection.2020
- Retracted
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Activated factor X is a key component of the coagulation cascade, but whether it directly regulates pathological cardiac remodeling is unclear. In mice subjected to pressure overload stress, cardiac factor X mRNA expression and activity increased concurrently with cardiac hypertrophy, fibrosis, inflammation and diastolic dysfunction, and responses blocked with a low coagulation-independent dose of rivaroxaban. In vitro, neurohormone stressors increased activated factor X expression in both cardiac myocytes and fibroblasts, resulting in activated factor X-mediated activation of protease-activated receptors and pro-hypertrophic and -fibrotic responses, respectively. Thus, inhibition of cardiac-expressed activated factor X could provide an effective therapy for the prevention of adverse cardiac remodeling in hypertensive patients.
Indexed as
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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.