Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity

Cardiorenal syndrome (CRS) represents a complex pathological interaction between the heart and the kidneys, where acute or chronic injury in one of them induces acute or chronic damage in the other. Out of the five subtypes, CRS type 1 (CRS-1), which is characterized by the worsening of cardiac func...

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Detalles Bibliográficos
Autor: Delgado Valero, Beatriz
Tipo de documento: Tesis doctoral
Fecha de publicación:2025
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Lenguaje:Inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/119052
Acceso en línea:https://hdl.handle.net/20.500.14352/119052
Nivel de acceso:Acceso abierto
Palabra clave:616.61(043.2)
Galectina
Nefrología y urología
3205.06 Nefrología
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author Delgado Valero, Beatriz
author_browse Delgado Valero, Beatriz
author_facet Delgado Valero, Beatriz
author_role author
collection Docta Complutense
description Cardiorenal syndrome (CRS) represents a complex pathological interaction between the heart and the kidneys, where acute or chronic injury in one of them induces acute or chronic damage in the other. Out of the five subtypes, CRS type 1 (CRS-1), which is characterized by the worsening of cardiac function leading to acute kidney injury [1], is known to have the highest incidence among the CRS diagnosed patients [2, 3]. Moreover, development of CRS-1 is known to increase hospitalization times and complicate clinical outcome in patients [4, 5].Although traditional cardiovascular risk factors such as hypertension, obesity or diabetes are believed to be implicated in the shared pathology of the heart and the kidneys, targeting only these factors in CRS-1 has shown unsatisfactory results [6], suggesting the need to assess non-conventional risk factors and other underlying mechanisms that could be relevant in the pathophysiology of CRS-induced renal damage...
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institution Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
language eng
network_acronym_str ES
network_name_str España
oai_identifier_str oai:docta.ucm.es:20.500.14352/119052
publishDate 2025
publishDateSort 2025
publisher Universidad Complutense de Madrid
publisherStr Universidad Complutense de Madrid
reponame_str Docta Complutense
spelling Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity La Galectina-3 promueve la activación del estrés de retículo endoplásmico a través de la disminución de let-7f-5p: relevancia en el daño renal post-infarto de miocardio en el contexto de la obesidad Delgado Valero, Beatriz 616.61(043.2) Galectina Nefrología y urología 3205.06 Nefrología Cardiorenal syndrome (CRS) represents a complex pathological interaction between the heart and the kidneys, where acute or chronic injury in one of them induces acute or chronic damage in the other. Out of the five subtypes, CRS type 1 (CRS-1), which is characterized by the worsening of cardiac function leading to acute kidney injury [1], is known to have the highest incidence among the CRS diagnosed patients [2, 3]. Moreover, development of CRS-1 is known to increase hospitalization times and complicate clinical outcome in patients [4, 5].Although traditional cardiovascular risk factors such as hypertension, obesity or diabetes are believed to be implicated in the shared pathology of the heart and the kidneys, targeting only these factors in CRS-1 has shown unsatisfactory results [6], suggesting the need to assess non-conventional risk factors and other underlying mechanisms that could be relevant in the pathophysiology of CRS-induced renal damage... Universidad Complutense de Madrid https://hdl.handle.net/20.500.14352/119052
spellingShingle Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
Delgado Valero, Beatriz
616.61(043.2)
Galectina
Nefrología y urología
3205.06 Nefrología
title Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
title_full Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
title_fullStr Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
title_full_unstemmed Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
title_short Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
title_sort Galectin-3 promotes endoplasmic reticulum stress via let-7f-5p down regulation: Relevance in renal damage post-myocardial infarction in the context of obesity
topic 616.61(043.2)
Galectina
Nefrología y urología
3205.06 Nefrología
topic_facet 616.61(043.2)
Galectina
Nefrología y urología
3205.06 Nefrología
url https://hdl.handle.net/20.500.14352/119052