ReviewJournal of cardiovascular development and disease2019
Ca
Review in Journal of cardiovascular development and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Pooled it
- Efficacy of tranilast in preventing exacerbating cardiac function and death from heart failure in muscular dystrophy patients with advanced-stage heart failure: a single-arm, open-label, multicenter study.Orphanet journal of rare diseases · 2025Trial
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Supraventricular Arrhythmias in Pulmonary Hypertension: A Comprehensive Review From Preclinical Evidence to Clinical Practice.Pulmonary circulation · 2026Review
- Next Generation Calcium Nanomaterials: Disrupting Tumor CaInternational journal of nanomedicine · 2026Review
- Calcium hydroxyapatite suppresses extracellular matrix-related gene expression by modulating Piezo1-associated CaAnimal cells and systems · 2026Article
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- Orai channel pharmacological manipulation reduces metabolic flexibility in cardiac fibroblasts.American journal of physiology. Cell physiology · 2025Article
- Magnetite Nanodiscs Activate Mechanotransductive Calcium Signaling in Diverse Cell Types.Journal of the American Chemical Society · 2025Article
- CaBiomedicines · 2025Review
- Long QT syndrome type 3 gain-of-function of NaCommunications biology · 2025Article
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- CaBiomolecules · 2024Review
- Pathophysiological Mechanisms of Psychosis-Induced Atrial Fibrillation: The Links between Mental Disorder and Arrhythmia.Reviews in cardiovascular medicine · 2024Review
- Versatile human cardiac tissues engineered with perfusable heart extracellular microenvironment for biomedical applications.Nature communications · 2024Article
- Microcurrent-Mediated Modulation of Myofibroblasts for Cardiac Repair and Regeneration.International journal of molecular sciences · 2024Article
- Editorial: Calcium regulation and Mechano-transduction in vascular diseases: obligatory role of transient receptor potential and Piezo channels.Frontiers in physiology · 2024Article
- Harnessing stem cell and lineage reprogramming technology to treat cardiac fibrosis.Cell regeneration (London, England) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac fibrosis is the excessive deposition of extracellular matrix proteins by cardiac fibroblasts and myofibroblasts, and is a hallmark feature of most heart diseases, including arrhythmia, hypertrophy, and heart failure. This maladaptive process occurs in response to a variety of stimuli, including myocardial injury, inflammation, and mechanical overload. There are multiple signaling pathways and various cell types that influence the fibrogenesis cascade. Fibroblasts and myofibroblasts are central effectors. Although it is clear that Ca
Indexed as
Identifiers
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.