ReviewTrends in pharmacological sciences2025
Cardiac fibrosis: from mechanisms and models to medicines.
Review in Trends in pharmacological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Review
- GPT2-mediated Glutamate to α-Ketoglutaric Acid Conversion in Cardiac Fibroblast Promotes Fibrosis.JACC. Basic to translational science · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Molecular Mechanisms of Cardiac Fibrosis: A Pathologist's Perspective.Current issues in molecular biology · 2026Review
- Killing of Gold Nanorods-Loaded Human Cardiac Fibroblasts Mediated by Photo-Thermal Activation.ACS omega · 2026Article
- Integrating mechanical cues inFrontiers in immunology · 2026Review
- Cardiometabolic Therapies Shape Non-Coding RNA Landscapes in Cardiovascular Fibrosis.Metabolites · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cardiac fibrosis is a hallmark of cardiovascular and systemic diseases that arises in diverse pathological contexts such as inflammation, metabolic stress, and mechanical overload. Despite its clinical relevance, no FDA-approved therapies directly target cardiac fibrotic remodeling, highlighting persistent challenges in disease organization, model fidelity, and translational strategy. Recent advances in human induced pluripotent stem cell (iPSC)-derived models, engineered heart tissues, and in vivo systems have uncovered new fibrotic drivers, including immune-stroma crosstalk, metabolic reprogramming, and mechanotransduction, that are reshaping therapeutic development. This review synthesizes emerging molecular mechanisms, experimental models, and preclinical and clinical investigations of antifibrotic agents. Distinct from previous reviews, we emphasize cross-contextual alignment to support the development of precision antifibrotic therapy for cardiac fibrosis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.