Preclinical scenario of targeting myocardial fibrosis with chimeric antigen receptor (CAR) immunotherapy

Fibrosis is present in an important proportion of myocardial disorders. Injury activates cardiac fibroblasts, which deposit excess extracellular matrix, increasing tissue stiffness, impairing cardiac function, and leading to heart failure. Clinical therapies that directly target excessive fibrosis a...

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Detalles Bibliográficos
Autores: Ferrer Curriu, Gemma, Soler Botija, Carolina, Charvatova, Sandra, Motais, Benjamin, Roura, Santiago, Gàlvez Montón, Carolina, Monguió Tortajada, Marta, Iborra Egea, Oriol, Emdin, Michele, Lupón, Josep, Aimo, Alberto, Bagó, Juli R., Genís, Antoni Bayés
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/193129
Acceso en línea:https://hdl.handle.net/2445/193129
Access Level:acceso abierto
Palabra clave:Miocardiopaties
Immunoteràpia
Fibroblasts
Myocardiopathies
Immunotheraphy
Descripción
Sumario:Fibrosis is present in an important proportion of myocardial disorders. Injury activates cardiac fibroblasts, which deposit excess extracellular matrix, increasing tissue stiffness, impairing cardiac function, and leading to heart failure. Clinical therapies that directly target excessive fibrosis are limited, and more effective treatments are needed. Immunotherapy based on chimeric antigen receptor (CAR) T cells is a novel technique that redirects T lymphocytes toward specific antigens to eliminate the target cells. It is currently used in haematological cancers but has demonstrated efficacy in mouse models of hypertensive cardiac fibrosis, with activated fibroblasts as the target cells. CAR T cell therapy is associated with significant toxicities, but CAR natural killer cells can overcome efficacy and safety limitations. The use of CAR immunotherapy offers a potential alternative to current therapies for fibrosis reduction and restoration of cardiac function in patients with myocardial fibrosis.