Evidence map›Paper›PMID 35204238›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Extracellular Vesicles in Redox Signaling and Metabolic Regulation in Chronic Kidney Disease.

Omar Emiliano Aparicio-Trejo, Ana Karina Aranda-Rivera, Horacio Osorio-Alonso, Elena Martínez-Klimova, Laura Gabriela Sánchez-Lozada, José Pedraza-Chaverri, Edilia Tapia

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  14. Extracellular vesicle-matrix interactions.Nature reviews. Materials · 2023
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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

7 authors at 2 institutions in 1 country.

Omar Emiliano Aparicio-TrejoDepartamento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City 14080, Mexico.ORCID 0000-0002-7701-4537
Ana Karina Aranda-RiveraLaboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0002-4095-754X
Horacio Osorio-AlonsoDepartamento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City 14080, Mexico.
Elena Martínez-KlimovaLaboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Laura Gabriela Sánchez-LozadaDepartamento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City 14080, Mexico.
José Pedraza-ChaverriLaboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0001-6628-4411
Edilia TapiaDepartamento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City 14080, Mexico.
Instituto Nacional de Cardiología · MXUniversidad Nacional Autónoma de México · MX

Funding

Consejo Nacional de Ciencia y Tecnología 281967Fondos de Gasto Directo Autorizados a la Subdirección de Investigación Básica del Instituto Nacional de Cardiología Ignacio Chávez 20200Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica (PAPIIT) IN200922
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a world health problem increasing dramatically. The onset of CKD is driven by several mechanisms; among them, metabolic reprogramming and changes in redox signaling play critical roles in the advancement of inflammation and the subsequent fibrosis, common pathologies observed in all forms of CKD. Extracellular vesicles (EVs) are cell-derived membrane packages strongly associated with cell-cell communication since they transfer several biomolecules that serve as mediators in redox signaling and metabolic reprogramming in the recipient cells. Recent studies suggest that EVs, especially exosomes, the smallest subtype of EVs, play a fundamental role in spreading renal injury in CKD. Therefore, this review summarizes the current information about EVs and their cargos' participation in metabolic reprogramming and mitochondrial impairment in CKD and their role in redox signaling changes. Finally, we analyze the effects of these EV-induced changes in the amplification of inflammatory and fibrotic processes in the progression of CKD. Furthermore, the data suggest that the identification of the signaling pathways involved in the release of EVs and their cargo under pathological renal conditions can allow the identification of new possible targets of injury spread, with the goal of preventing CKD progression.

Indexed as

chronic kidney diseaseexosomesextracellular vesiclesfibrosisinflammationlipotoxicitymetabolic reprogrammingmicrovesiclesmitochondrial impairmentoxidative stressredox signaling

Identifiers

PMID35204238
PMCPMC8868440
OpenAlexW4211158222

What OpenQuestion 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 OpenQuestion graph.