ArticleJCI insight2021
Serum circulating proteins from pediatric patients with dilated cardiomyopathy cause pathologic remodeling and cardiomyocyte stiffness.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Identification of diagnostic and therapeutic roles of programmed cell death-related proteins in dilated cardiomyopathy: a multi-omics and experimental validation study.Scientific reports · 2026Article
- Region-specific human cardiac extracellular vesicles differentially regulate mitochondrial function.Extracellular vesicles and circulating nucleic acids · 2026Article
- Human fetal circulating factors from pregnancies complicated by obesity upregulate genes associated with pathological hypertrophy in neonatal rat cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2026Article
- A novel Notch and WNT signaling mechanism contribute to paediatric DCM: a pathway to new therapeutics.bioRxiv : the preprint server for biology · 2025Article
- The pericardium forms as a distinct structure during heart formation.Nature communications · 2025Article
- Midkine Serum Levels in Inflammatory and Non-Inflammatory Dilated Cardiomyopathy.Biomedicines · 2025Article
- Circulating and Cardiac Tissue miRNAs in Children with Dilated Cardiomyopathy.Journal of cardiovascular development and disease · 2023Article
- The secretome as a biomarker and functional agent in heart failure.The journal of cardiovascular aging · 2023Article
- Hydroxychloroquine Mitigates Dilated Cardiomyopathy Phenotype in Transgenic D94A Mice.International journal of molecular sciences · 2022Article
- Atomic Force Microscopy (AFM) Applications in Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Integrative bioinformatics analysis of potential therapeutic targets and immune infiltration characteristics in dilated cardiomyopathy.Annals of translational medicine · 2022Article
- RBM20, a Therapeutic Target to Alleviate Myocardial StiffnessFrontiers in cardiovascular medicine · 2022Review
- Multiple-model machine learning identifies potential functional genes in dilated cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Midkine-A novel player in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remain limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with serum from nonfailing or DCM pediatric patients activates the fetal gene program (FGP). Here we show that serum treatment with proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating miRNAs, promote these pathological changes. Evaluation of the protein secretome showed that midkine (MDK) is upregulated in DCM serum, and NRVM treatment with MDK activates the FGP. Changes in gene expression in serum-treated NRVMs, evaluated by next-generation RNA-Seq, indicated extracellular matrix remodeling and focal adhesion pathways were upregulated in pediatric DCM serum and in DCM serum-treated NRVMs, suggesting alterations in cellular stiffness. Cellular stiffness was evaluated by Atomic Force Microscopy, which showed an increase in stiffness in DCM serum-treated NRVMs. Of the proteins increased in DCM sera, secreted frizzled-related protein 1 (sFRP1) was a potential candidate for the increase in cellular stiffness, and sFRP1 treatment of NRVMs recapitulated the increase in cellular stiffness observed in response to DCM serum treatment. Our results show that serum circulating proteins promoted pathological changes in gene expression and cellular stiffness, and circulating miRNAs were protective against pathological changes.
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