ArticleCirculation research2024
Targeting Cyclophilin A in the Cardiac Microenvironment Preserves Heart Function and Structure in Failing Hearts.
Article in Circulation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Extracellular cyclophilin A promotes B-cell acute lymphoblastic leukemia progression via MC2R.EMBO molecular medicine · 2026Article
- Multi-omics analysis of histidine metabolism reveals FRZB-CRYM-associated cellular crosstalk in heart failure.Frontiers in cardiovascular medicine · 2026Article
- Cyclophilin B deficiency enhances myocardial energy synthesis and protects against heart failure in preclinical models.BMC medicine · 2025Article
- Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025Review
- Mitophagy in Hypertensive Cardiac Hypertrophy: Mechanisms and Therapeutic Implications.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- Nanotechnology meets medicine: applications of atomic force microscopy in disease.Biophysical reviews · 2025Review
- Cyclophilin(g) a Knowledge Gap in Heart Failure Pathogenesis.Circulation research · 2024Article
- Brain cell-released Cyclophilin A induces neuroinflammation and exacerbates blood-brain barrier injury in acute ischemic stroke.Frontiers in neurologyArticle
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23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac hypertrophy is characterized by remodeling of the myocardium, which involves alterations in the ECM (extracellular matrix) and cardiomyocyte structure. These alterations critically contribute to impaired contractility and relaxation, ultimately leading to heart failure. Emerging evidence implicates that extracellular signaling molecules are critically involved in the pathogenesis of cardiac hypertrophy and remodeling. The immunophilin CyPA (cyclophilin A) has been identified as a potential culprit. In this study, we aimed to unravel the interplay between eCyPA (extracellular CyPA) and myocardial dysfunction and evaluate the therapeutic potential of inhibiting its extracellular accumulation to improve heart function.
methodsEmploying a multidisciplinary approach encompassing in silico, in vitro, in vivo, and ex vivo experiments we studied a mouse model of cardiac hypertrophy and human heart specimen to decipher the interaction of CyPA and the cardiac microenvironment in highly relevant pre-/clinical settings. Myocardial expression of CyPA (immunohistology) and the inflammatory transcriptome (NanoString) was analyzed in human cardiac tissue derived from patients with nonischemic, noninflammatory congestive heart failure (n=187). These analyses were paralleled by a mouse model of Ang (angiotensin) II-induced heart failure, which was assessed by functional (echocardiography), structural (immunohistology, atomic force microscopy), and biomolecular (Raman spectroscopy) analyses. The effect of inhibiting eCyPA in the cardiac microenvironment was evaluated using a newly developed neutralizing anti-eCyPA monoclonal antibody.
resultsWe observed a significant accumulation of eCyPA in both human and murine-failing hearts. Importantly, higher eCyPA expression was associated with poor clinical outcomes in patients (
conclusionsOur study provides strong evidence of the pathogenic role of eCyPA in remodeling, myocardial stiffening, and dysfunction in heart failure. The findings suggest that antibody-based inhibition of eCyPA may offer a novel therapeutic strategy for nonischemic heart failure. Further research is needed to evaluate the translational potential of these interventions in human patients with cardiac hypertrophy.
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