Evidence map›Paper›PMID 32266265›Full record

ReviewFrontiers in cell and developmental biology2020

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

Julia Carracedo, Matilde Alique, Carmen Vida, Guillermo Bodega, Noemí Ceprián, Enrique Morales, Manuel Praga, Patricia de Sequera, Rafael Ramírez

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 1 synthesis or guideline pooled it.

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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Julia CarracedoDepartamento de Genética, Fisiología y Microbiología, Universidad Complutense/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Matilde AliqueDepartamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.
Carmen VidaDepartamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.
Guillermo BodegaDepartamento de Biomedicina y Biotecnología, Facultad de Biología, Química y Ciencias Ambientales, Universidad de Alcalá, Alcalá de Henares, Spain.
Noemí CepriánDepartamento de Genética, Fisiología y Microbiología, Universidad Complutense/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Enrique MoralesDepartamento de Nefrología, Hospital Universitario 12 de Octubre/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Manuel PragaDepartamento de Nefrología, Hospital Universitario 12 de Octubre/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.
Patricia de SequeraDepartamento de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Rafael RamírezDepartamento Biología de Sistemas, Facultad de Medicina y Ciencias de la Salud (IRYCIS), Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

atherosclerosiscardiovascular diseasescellular senescencechronic kidney diseaseepigenetic alterationsextracellular vesiclesmicroRNAsreactive oxygen species

Identifiers

PMID32266265
PMCPMC7099607

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.