Mechanisms of Cardiovascular Disorders in Patients With Chronic Kidney Disease: A Process Related to Accelerated Senescence.

atherosclerosis cardiovascular diseases cellular senescence chronic kidney disease epigenetic alterations extracellular vesicles microRNAs reactive oxygen species

Journal

Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250

Informations de publication

Date de publication:
2020
Historique:
received: 18 12 2019
accepted: 05 03 2020
entrez: 9 4 2020
pubmed: 9 4 2020
medline: 9 4 2020
Statut: epublish

Résumé

Cardiovascular diseases (CVDs), especially those involving a systemic inflammatory process such as atherosclerosis, remain the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD). CKD is a systemic condition affecting approximately 10% of the general population. The prevalence of CKD has increased over the past decades because of the aging of the population worldwide. Indeed, CVDs in patients with CKD constitute a premature form of CVD observed in the general population. Multiple studies indicate that patients with renal disease undergo accelerated aging, which precipitates the appearance of pathologies, including CVDs, usually associated with advanced age. In this review, we discuss several aspects that characterize CKD-associated CVDs, such as etiopathogenic elements that CKD patients share with the general population, changes in the cellular balance of reactive oxygen species (ROS), and the associated process of cellular senescence. Uremia-associated aging is linked with numerous changes at the cellular and molecular level. These changes are similar to those observed in the normal process of physiologic aging. We also discuss new perspectives in the study of CKD-associated CVDs and epigenetic alterations in intercellular signaling, mediated by microRNAs and/or extracellular vesicles (EVs), which promote vascular damage and subsequent development of CVD. Understanding the processes and factors involved in accelerated senescence and other abnormal intercellular signaling will identify new therapeutic targets and lead to improved methods of diagnosis and monitoring for patients with CKD-associated CVDs.

Identifiants

pubmed: 32266265
doi: 10.3389/fcell.2020.00185
pmc: PMC7099607
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

185

Informations de copyright

Copyright © 2020 Carracedo, Alique, Vida, Bodega, Ceprián, Morales, Praga, de Sequera and Ramírez.

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Auteurs

Julia Carracedo (J)

Departamento de Genética, Fisiología y Microbiología, Universidad Complutense/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.

Matilde Alique (M)

Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.

Carmen Vida (C)

Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.

Guillermo Bodega (G)

Departamento de Biomedicina y Biotecnología, Facultad de Biología, Química y Ciencias Ambientales, Universidad de Alcalá, Alcalá de Henares, Spain.

Noemí Ceprián (N)

Departamento de Genética, Fisiología y Microbiología, Universidad Complutense/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.

Enrique Morales (E)

Departamento de Nefrología, Hospital Universitario 12 de Octubre/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Departamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain.

Manuel Praga (M)

Departamento de Nefrología, Hospital Universitario 12 de Octubre/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Departamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain.

Patricia de Sequera (P)

Departamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Sección de Nefrología, Hospital Universitario Infanta Leonor, Madrid, Spain.

Rafael Ramírez (R)

Departamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.

Classifications MeSH