Cardiac Remodeling in Chronic Kidney Disease.
cardiac fibrosis
cardiorenal syndrome
chronic kidney disease
heart failure
left-ventricular hypertrophy
organ crosstalk
uremia
uremic cardiomyopathy
Journal
Toxins
ISSN: 2072-6651
Titre abrégé: Toxins (Basel)
Pays: Switzerland
ID NLM: 101530765
Informations de publication
Date de publication:
05 03 2020
05 03 2020
Historique:
received:
17
02
2020
revised:
02
03
2020
accepted:
03
03
2020
entrez:
11
3
2020
pubmed:
11
3
2020
medline:
2
3
2021
Statut:
epublish
Résumé
Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
Identifiants
pubmed: 32150864
pii: toxins12030161
doi: 10.3390/toxins12030161
pmc: PMC7150902
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
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