Evidence map›Paper›PMID 36358557›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Involvement of Mitochondrial Dysfunction in the Inflammatory Response in Human Mesothelial Cells from Peritoneal Dialysis Effluent.

Olalla Ramil-Gómez, Mirian López-Pardo, Jennifer Adriana Fernández-Rodríguez, Ana Rodríguez-Carmona, Teresa Pérez-López, Carlos Vaamonde-García, Miguel Pérez-Fontán, María José López-Armada

Open access · goldAbstract read
In one paragraph

Article 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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Olalla Ramil-GómezAging and Inflammation Research Laboratory, Institute for Biomedical Research of A Coruña (INIBIC), 15006 A Coruña, Spain.
Mirian López-PardoAging and Inflammation Research Laboratory, Institute for Biomedical Research of A Coruña (INIBIC), 15006 A Coruña, Spain.
Jennifer Adriana Fernández-RodríguezAging and Inflammation Research Laboratory, Institute for Biomedical Research of A Coruña (INIBIC), 15006 A Coruña, Spain.
Ana Rodríguez-CarmonaAging and Inflammation Research Laboratory, Institute for Biomedical Research of A Coruña (INIBIC), 15006 A Coruña, Spain.
Teresa Pérez-LópezDivision of Nephrology, University Hospital A Coruña (CHUAC), 15006 A Coruña, Spain.
Carlos Vaamonde-GarcíaRheumatology Research Group, INIBIC, CHUAC, 15006 A Coruña, Spain.ORCID 0000-0001-8658-5502
Miguel Pérez-FontánEndocrine, Nutritional and Metabolic Diseases Group, Faculty of Health Sciences, A Coruña, INIBIC, 15006 A Coruña, Spain.
María José López-ArmadaAging and Inflammation Research Laboratory, Institute for Biomedical Research of A Coruña (INIBIC), 15006 A Coruña, Spain.ORCID 0000-0001-5325-6251
Instituto de Investigación Biomédica de A Coruña · ESUniversidade da Coruña · ESComplexo Hospitalario Universitario A Coruña · ESi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PT

Funding

Fundación Eugenio Rodríguez Pascual Convocatoria 2021Instituto de Salud Carlos III PI15/02218 and PI18/01803
6 · The paper itself

Abstract

Recent studies have related mitochondrial impairment with peritoneal membrane damage during peritoneal dialysis (PD) therapy. Here, we assessed the involvement of mitochondrial dysfunction in the inflammatory response in human mesothelial cells, a hallmark in the pathogenesis of PD-related peritoneal membrane damage. Our ex vivo studies showed that IL-1β causes a drop in the mitochondrial membrane potential in cells from peritoneal effluent. Moreover, when mitochondrial damage was induced by inhibitors of mitochondrial function, a low-grade inflammatory response was generated. Interestingly, mitochondrial damage sensitized mesothelial cells, causing a significant increase in the inflammatory response induced by cytokines, in which ROS generation and NF-κB activation appear to be involved, since inflammation was counteracted by both mitoTEMPO (mitochondrial ROS scavenger) and BAY-117085 (NF-κB inhibitor). Furthermore, the natural anti-inflammatory antioxidant resveratrol significantly attenuated the inflammatory response, by reversing the decline in mitochondrial membrane potential and decreasing the expression of IL-8, COX-2 and PGE

Indexed as

inflammationmesothelial cellsmitochondriaoxidative stressperitoneal dialysisresveratrol

Identifiers

PMID36358557
PMCPMC9686714
OpenAlexW4308444841

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.