ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
Claudin-5 levels are reduced from multiple cell types in human failing hearts and are associated with mislocalization of ephrin-B1.
Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Claudin 5 Across the Vascular Landscape: From Blood-Tissue Barrier Regulation to Disease Mechanisms.Cells · 2025Review
- Discovery ofDiagnostics (Basel, Switzerland) · 2025Article
- Recent advances of the Ephrin and Eph family in cardiovascular development and pathologies.iScience · 2024Review
- A Simple and Effective Method to Consistently Isolate Mouse Cardiomyocytes.Journal of visualized experiments : JoVE · 2022Article
- Myocardial oedema: pathophysiological basis and implications for the failing heart.ESC heart failure · 2022Review
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- A Novel Role of Claudin-5 in Prevention of Mitochondrial Fission Against Ischemic/Hypoxic Stress in Cardiomyocytes.The Canadian journal of cardiology · 2021Article
- Micro-dystrophin gene therapy prevents heart failure in an improved Duchenne muscular dystrophy cardiomyopathy mouse model.JCI insight · 2021Article
- In the line-up: deleted genes associated with DiGeorge/22q11.2 deletion syndrome: are they all suspects?Journal of neurodevelopmental disorders · 2019Review
- Claudin-5: gatekeeper of neurological function.Fluids and barriers of the CNS · 2019Review
- Impairment of blood-brain barrier is an early event in R6/2 mouse model of Huntington Disease.Scientific reports · 2017Article
- Limited beneficial effects of piceatannol supplementation on obesity complications in the obese Zucker rat: gut microbiota, metabolic, endocrine, and cardiac aspects.Journal of physiology and biochemistry · 2016Article
- Duchenne Muscular Dystrophy Mice and Men: Can Understanding a Genetic Cardiomyopathy Inform Treatment of Other Myocardial Diseases?Circulation research · 2016Article
- Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy.Frontiers in physiology · 2016Article
- Altered protein levels in the isolated extracellular matrix of failing human hearts with dilated cardiomyopathy.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
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12 authors at 1 institution in 1 country.
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Abstract
Claudin-5 is transcriptionally downregulated resulting in dramatically reduced protein levels in human heart failure. Studies in mice have demonstrated that reduced claudin-5 levels occur prior to cardiac damage and far before reduced whole heart function. Therefore, claudin-5 may be a useful early therapeutic target for human heart failure. However, the cell types in which claudin-5 is localized in human heart and from which claudin-5 is reduced in heart failure is not known. The recent identification of claudin-5's interaction with ephrin-B1 in mouse hearts has also not been investigated in non-failing or failing human hearts. In this study we collected human left ventricular mid-myocardium histological samples from 7 non-failing hearts and 16 end-stage failing hearts. Immunoblots demonstrate severe reductions of claudin-5 protein in 14 of 16 failing hearts compared to non-failing controls. Claudin-5 was observed to localize to cardiomyocytes, endothelial cells, and a subset of fibroblasts in non-failing human heart sections. In isolated cardiomyocytes, the transmembrane claudin-5 protein localized in longitudinal striations in lateral membranes. In failing heart, both cardiomyocyte and endothelial claudin-5 localization was severely reduced, but claudin-5 remained in fibroblasts. Absence of claudin-5 staining also correlated with the reduction of the endothelial cell marker CD31. Ephrin-B1 localization, but not protein levels, was altered in failing hearts supporting that claudin-5 is required for ephrin-B1 localization. These data support that loss of claudin-5 in cardiomyocytes and endothelial cells is prevalent in human heart failure. Investigating claudin-5/ephrin-B1 protein complexes and gene regulation may lead to novel therapies.
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