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A rift has opened and is widening between basic research (bench) and clinical research and patients (bed) who need their new treatments, diagnostics and preventive strategies. This problem involving the 'translation' of basic scientific findings into clinical applications and potential treatments or biomarkers for a condition like heart failure is widely recognized both in academia and industry. Despite the attempts that have been made by both sides to improve this situation, the high attrition rates of drug development and the problem with reproducibility and translatability of preclinical findings to human applications still persist. As a result, the return on investment of basic research has been limited in terms of clinical impact. In this scientific statement we describe and discuss various issues with relevance to this theme and try to dissect how to move our field towards the development of more effective heart failure drugs. We zoom in on facilitating the process of heart failure drug development, the unnecessary gaps ('valley of death') between the critical steps in heart failure drug development, validation and de-validation of new concepts as early as possible ('rigorous translation'). We describe forums on how to stimulate cross-talk and interaction between clinician-scientists, basic heart failure researchers, biotech and industry, and how to enable them to speak the same language, and lessons learned from successes outside the heart failure field.
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http://dx.doi.org/10.1002/ejhf.3709 | DOI Listing |
J Palliat Care
September 2025
Department of Healthcare Administration and Policy, School of Public Health, University of Nevada, Las Vegas, NV, USA.
ObjectivesRecently, atrial fibrillation (AF) has contributed to an increase in cardiovascular deaths in the U.S. Palliative care (PC) and atrial ablation (AA) procedure can elevate quality of life of high-risk AF patients, who are associated with multiple comorbidities.
View Article and Find Full Text PDFPLoS One
September 2025
Biobank of Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, PR China.
Heart failure (HF) and lung cancer (LC) often coexist, yet their shared molecular mechanisms are unclear. We analyzed transcriptome data from the NCBI Gene Expression Omnibus (GEO) database (GSE141910, GSE57338) to identify 346 HF‑related differentially expressed genes (DEGs), then combined weighted gene co-expression network analysis (WGCNA) pinpointed 70 hub candidates. Further screening of these 70 hub candidates in TCGA lung cancer cohorts via LASSO, Random Forest, and multivariate Cox regression suggested CYP4B1 as the only independent prognostic marker.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiology, Fuzhou University Affiliated Provincial Hospital, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Introduction: Kidney stone disease is associated with numerous cardiovascular risk factors. However, the findings across studies are non-uniformly consistent, and the control of confounding variables remains suboptimal. This study aimed to investigate the association between kidney stone and cardiovascular disease.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Division of Pediatric Critical Care, Department of Pediatrics, University of California, San Francisco, USA.
Right ventricular (RV) failure is the primary cause of death among patients with pulmonary arterial hypertension (PAH). Patients with congenital heart disease-associated PAH (CHD-PAH) demonstrate improved outcomes compared to patients with other forms of PAH, which is related to the maintenance of an adaptively hypertrophied RV. In an ovine model of CHD-PAH, we aimed to elucidate the cellular, microvascular, and transcriptional adaptations to congenital pressure overload that support RV function.
View Article and Find Full Text PDFJCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
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