Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications

Heart failure (HF) remains a major global health challenge defined by the inability of the heart to adequately meet systemic metabolic requirements. While ventricular dysfunction has traditionally been the primary focus in both conceptual and clinical frameworks of HF, emerging evidence highlights a...

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Autores: Gil Fernández, Marta, Bueno Sen, Andrea, Cantolla Pablo, Paula, Val Blasco, Almudena, Ruiz Hurtado, Gema, Delgado, Carmen, Cubillos, Carolina, Boscá Gomar, Lisardo, Fernández Velasco, María
Formato: artículo
Fecha de publicación:2025
País:España
Recursos:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:dnet:biblosearchi::42933e594b368e0319bb1aeee0b8808b
Acesso em linha:https://hdl.handle.net/10486/778580
https://dx.doi.org/10.3390/ijms26178210
Access Level:acceso abierto
Palavra-chave:atrial myopathy
heart failure
inflammation
innate immunity
Medicina
Química
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spelling Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implicationsGil Fernández, MartaBueno Sen, AndreaCantolla Pablo, PaulaVal Blasco, AlmudenaRuiz Hurtado, GemaDelgado, CarmenCubillos, CarolinaBoscá Gomar, LisardoFernández Velasco, Maríaatrial myopathyheart failureinflammationinnate immunityMedicinaQuímicaHeart failure (HF) remains a major global health challenge defined by the inability of the heart to adequately meet systemic metabolic requirements. While ventricular dysfunction has traditionally been the primary focus in both conceptual and clinical frameworks of HF, emerging evidence highlights atrial myopathy—covering structural, functional, electrical, metabolic, and neurohormonal remodeling—as a central yet often overlooked contributor to disease progression across the HF spectrum. This review offers a comprehensive overview of the molecular and cellular mechanisms underlying atrial remodeling, with a focus on inflammation and innate immune activation as key pathogenic mediators. Among pattern recognition receptors, Toll-like receptors (TLRs) and NOD-like receptors (NLRs) play crucial roles in translating myocardial stress into pro-inflammatory, profibrotic, and pro-arrhythmic signals that exacerbate HF. By combining experimental and clinical evidence, we emphasize atrial myopathy as both a biomarker and an active driver of HF deterioration, advocating for the inclusion of atrial-targeted diagnostics and immunomodulatory therapies in future HF treatment approaches. Such a paradigm shift holds significant potential for improved risk stratification, arrhythmia prevention, attenuation of structural remodeling, and ultimately, better prognosis and clinical outcomes in this increasingly common syndromeThis work was funded by the Spanish Ministry of Science and Innovation (MICIN/AEI/10.13039/501100011033) through grants PID2023-148933OB-I00 and CNS2023-145161, and the REDINFLAMA network (grant RED2022-134511-T); by the Instituto de Salud Carlos III (ISCIII) through grants PI20/01482, PI23/01014, F21/00259, CM23/00121, CD22/00055, PMP22/00098, PT23/00028, and by CIBERCV (Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares). Funding was also provided by the European Regional Development Fund (ERDF), the European Social Fund (ESF), and the COMETA-Red (Consejo Superior de Investigaciones Científicas, CSIC). Additional support was provided by the Spanish Society of Cardiology—Translational Project 2019, and the Heart Rhythm Association (SEC, Spain) through the Asociación Insuficiencia Cardiaca (Trasplante Cardiaco) Project 20203. A.V.B. was supported by a Sara Borrell postdoctoral fellowship (CD22/00055), funded by the Instituto de Salud Carlos III (ISCIII), the European Union—NextGenerationEU, and the Spanish Recovery, Transformation and Resilience Plan (PRTR)MDPIDepartamento de FisiologíaFacultad de MedicinaGobierno de EspañaAgencia Estatal de InvestigaciónInstituto de Salud Carlos III20252025-08-24review articlehttp://purl.org/coar/resource_type/c_dcae04bcVoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/10486/778580https://dx.doi.org/10.3390/ijms2617821040943136reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2Attribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:dnet:biblosearchi::42933e594b368e0319bb1aeee0b8808b2026-06-23T12:46:27Z
dc.title.none.fl_str_mv Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
title Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
spellingShingle Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
Gil Fernández, Marta
atrial myopathy
heart failure
inflammation
innate immunity
Medicina
Química
title_short Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
title_full Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
title_fullStr Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
title_full_unstemmed Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
title_sort Atrial myopathy and heart failure: Immunomolecular mechanisms and clinical implications
dc.creator.none.fl_str_mv Gil Fernández, Marta
Bueno Sen, Andrea
Cantolla Pablo, Paula
Val Blasco, Almudena
Ruiz Hurtado, Gema
Delgado, Carmen
Cubillos, Carolina
Boscá Gomar, Lisardo
Fernández Velasco, María
author Gil Fernández, Marta
author_facet Gil Fernández, Marta
Bueno Sen, Andrea
Cantolla Pablo, Paula
Val Blasco, Almudena
Ruiz Hurtado, Gema
Delgado, Carmen
Cubillos, Carolina
Boscá Gomar, Lisardo
Fernández Velasco, María
author_role author
author2 Bueno Sen, Andrea
Cantolla Pablo, Paula
Val Blasco, Almudena
Ruiz Hurtado, Gema
Delgado, Carmen
Cubillos, Carolina
Boscá Gomar, Lisardo
Fernández Velasco, María
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Departamento de Fisiología
Facultad de Medicina
Gobierno de España
Agencia Estatal de Investigación
Instituto de Salud Carlos III
dc.subject.none.fl_str_mv atrial myopathy
heart failure
inflammation
innate immunity
Medicina
Química
topic atrial myopathy
heart failure
inflammation
innate immunity
Medicina
Química
description Heart failure (HF) remains a major global health challenge defined by the inability of the heart to adequately meet systemic metabolic requirements. While ventricular dysfunction has traditionally been the primary focus in both conceptual and clinical frameworks of HF, emerging evidence highlights atrial myopathy—covering structural, functional, electrical, metabolic, and neurohormonal remodeling—as a central yet often overlooked contributor to disease progression across the HF spectrum. This review offers a comprehensive overview of the molecular and cellular mechanisms underlying atrial remodeling, with a focus on inflammation and innate immune activation as key pathogenic mediators. Among pattern recognition receptors, Toll-like receptors (TLRs) and NOD-like receptors (NLRs) play crucial roles in translating myocardial stress into pro-inflammatory, profibrotic, and pro-arrhythmic signals that exacerbate HF. By combining experimental and clinical evidence, we emphasize atrial myopathy as both a biomarker and an active driver of HF deterioration, advocating for the inclusion of atrial-targeted diagnostics and immunomodulatory therapies in future HF treatment approaches. Such a paradigm shift holds significant potential for improved risk stratification, arrhythmia prevention, attenuation of structural remodeling, and ultimately, better prognosis and clinical outcomes in this increasingly common syndrome
publishDate 2025
dc.date.none.fl_str_mv 2025
2025-08-24
dc.type.none.fl_str_mv review article
http://purl.org/coar/resource_type/c_dcae04bc
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/10486/778580
https://dx.doi.org/10.3390/ijms26178210
40943136
url https://hdl.handle.net/10486/778580
https://dx.doi.org/10.3390/ijms26178210
identifier_str_mv 40943136
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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