ReviewNature reviews. Cardiology2020
Heart failure as interstitial cancer: emergence of a malignant fibroblast phenotype.
Review in Nature reviews. Cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 49 citations in OpenAlex.
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Cardiac Myofibroblast-Derived Small Extracellular Vesicles Moderate Fibrotic Responses via piRNA-62788/PIWIL2-Mediated SRF Silencing.Journal of extracellular vesicles · 2025Article
- A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling.Nature communications · 2025Article
- Application ofMedComm · 2025Article
- Cancer Development and Progression in Patients with Heart Failure.Current heart failure reports · 2024Review
- Identification of fibrosis-associated biomarkers in heart failure and human cancers.Journal of translational medicine · 2024Article
- The Role of Programmed Types of Cell Death in Pathogenesis of Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Review
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
- Cardiac sympathetic overdrive, M2 macrophage activation and fibroblast heterogeneity are associated with cardiac remodeling in a chronic pressure overload rat model of HFpEF.Frontiers in pharmacology · 2024Article
- Porcupine inhibitor CGX1321 alleviates heart failure with preserved ejection fraction in mice by blocking WNT signaling.Acta pharmacologica Sinica · 2023Article
- Visualization of Activated Fibroblasts in Heart Failure with Preserved Ejection Fraction with [Molecular pharmaceutics · 2023Article
- CRISPR-Cas9 editing of TLR4 to improve the outcome of cardiac cell therapy.Scientific reports · 2023Article
- Obesity-Associated ECM Remodeling in Cancer Progression.Cancers · 2022Review
- Aminoacylase-1 plays a key role in myocardial fibrosis and the therapeutic effects of 20(S)-ginsenoside Rg3 in mouse heart failure.Acta pharmacologica Sinica · 2022Article
- The RalGAPα1-RalA signal module protects cardiac function through regulating calcium homeostasis.Nature communications · 2022Article
- Preclinical platforms to study therapeutic efficacy of human γδ T cells.Clinical and translational medicine · 2022Article
- Ongoing Clinical Trials in Aging-Related Tissue Fibrosis and New Findings Related to AhR Pathways.Aging and disease · 2022Review
- Immuno-cardio-oncology: Killing two birds with one stone?Frontiers in immunology · 2022Review
- Integrated Bioinformatics IdentifiesApplied bionics and biomechanics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A prolonged state of left ventricular pressure overload, commonly caused by hypertension and aortic valve disease, promotes remodelling of the myocardium that can progress to heart failure with preserved ejection fraction (HFpEF). In animal models, a major factor driving progression from pressure-overload hypertrophy (POH) to HFpEF is the activation and proliferation of an abnormal fibroblast phenotype that is resistant to apoptosis, degrades normal stromal matrix and is replaced with a fibrotic matrix structure. A similar fibroblast phenotype has been identified in the stroma of solid cancers. This cancer-associated fibroblast drives tumour growth and invasion. The proliferation and expansion of these abnormal fibroblast populations in both HFpEF and cancer contribute to progression of disease. In early-phase clinical trials, chemotherapeutic agents targeting cancer-associated fibroblasts had antitumour properties. In this Perspectives article, we postulate that, because the abnormal fibroblast populations in POH and cancer have identical characteristics, chemotherapeutic agents targeting the POH-related fibroblast might attenuate the development of myocardial fibrosis, a pathophysiological hallmark of HFpEF. These agents must be designed to target the abnormal fibroblasts with high specificity because many classes of chemotherapeutic drugs can themselves cause myocardial dysfunction and heart failure.
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.