ReviewPharmaceuticals (Basel, Switzerland)2024
Hitting the Target! Challenges and Opportunities for TGF-β Inhibition for the Treatment of Cardiac fibrosis.
Review in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 26 citations in OpenAlex.
- Cardiac Fibrosis as a Dynamic Therapeutic Target: Overcoming Translational Barriers to Antifibrotic Therapy.JACC. Basic to translational science · 2026Review
- Review
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Heart failure may promote breast cancer progression through a Col10a1-associated Tgf-β/Smad-EMT pathway.Biology direct · 2026Article
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Mathematical Modeling of Systemic Sclerosis and Its Treatment.Bulletin of mathematical biology · 2026Article
- Preclinical evaluation of cysteine protease-inhibitor aloxistatin (E64d) for heart failure therapy.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- Myocardial Fibrosis in Cardiovascular Disease: An Integrative Biomarker-Imaging Framework Linking Molecular Mechanisms to Structural Phenotypes.Journal of clinical medicine · 2026Review
- ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.International journal of molecular sciences · 2026Article
- Review
- Cardiomyocyte-derived TGFB3 attenuates cardiac fibrosis and preserves cardiac function in heart failure.Scientific reports · 2026Article
- Disruption of the Fibroinflammatory Loop: A Therapeutic Strategy for Cardiac Fibrosis in Non-Ischemic Cardiomyopathy.Reviews in cardiovascular medicine · 2026Article
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- Review
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Dopamine agonist-associated fibrosis in prolactinomas: clinical challenges, impacts on the tumor microenvironment, and future directions.Frontiers in endocrinology · 2026Review
- Recent Updates on Molecular and Physical Therapies for Organ Fibrosis.Molecules (Basel, Switzerland) · 2025Review
- Signaling pathway alterations in hearts of a porcine model harboring a β-myosin heavy chain (MYH7-R403Q) gene variant.Journal of molecular and cellular cardiology plus · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developing effective anti-fibrotic therapies for heart diseases holds the potential to address unmet needs in several cardiac conditions, including heart failure with preserved ejection fraction, hypertrophic cardiomyopathy, and cardiotoxicity induced by cancer therapy. The inhibition of the primary fibrotic regulator, transforming growth factor (TGF) β, represents an efficient strategy for mitigating fibrosis in preclinical models. However, translating these findings into clinical benefits faces challenges due to potential adverse effects stemming from TGF-β's physiological actions in inflammation and tissue homeostasis. Various strategies exist for inhibiting TGF-β, each associated with a distinct risk of adverse effects. Targeting TGF-β directly or through its signaling pathway proves efficient in reducing fibrosis. However, direct TGF-β blockade may lead to uncontrolled inflammation, especially following myocardial infarction, while interference with the signaling pathway may compromise structural integrity, resulting in issues like insufficient wound healing or ventricular dilatation. Influencing TGF-β activity through interacting signaling pathways, for instance by inhibitors of the renin-angiotensin-aldosterone-system, is insufficiently potent in reducing fibrosis. Targeting activators of latent TGF-β, including ADAMTS enzymes, thrombospondin, and integrins, emerges as a potentially safer strategy to reduce TGF-β-induced fibrosis but it requires the identification of appropriate targets. Encouragement is drawn from promising agents developed for fibrosis in other organs, fueling hope for similar breakthroughs in treating cardiac fibrosis. Such advances depend on overcoming obstacles for the implementation of anti-fibrotic strategies in patients with heart disease, including fibrosis quantification. In this review, insights garnered from interventional and mechanistic studies, obtained through a non-systemic search spanning preclinical and clinical evidence, are summarized to pinpoint the most promising targets for further exploration and development.
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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.