Evidence map›Paper›PMID 35204184›Full record

ArticleAntioxidants (Basel, Switzerland)2022

Oxidative Stress and Cellular Senescence Are Involved in the Aging Kidney.

Laura Marquez-Exposito, Lucia Tejedor-Santamaria, Floris A Valentijn, Antonio Tejera-Muñoz, Sandra Rayego-Mateos, Vanessa Marchant, Raul R Rodrigues-Diez, Irene Rubio-Soto, Sebastiaan N Knoppert, Alberto Ortiz and 3 more

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 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
18.6field-weighted citation impact, top 1% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. AAV-mediated FGF21 gene therapy promotes health span extension by whole-body tissue-specific adaptations.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  4. SGLT2 Inhibition Attenuates Renal Tubular Senescence by Suppressing CTRP1-Mediated Glucotoxic Stress in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  15. Review
  16. Canine-derivedCurrent research in microbial sciences · 2025
    Article
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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

13 authors at 2 institutions in 3 countries.

Laura Marquez-ExpositoCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.ORCID 0000-0003-4812-1939
Lucia Tejedor-SantamariaCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.ORCID 0000-0003-4295-7284
Floris A ValentijnDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.ORCID 0000-0003-3676-6596
Antonio Tejera-MuñozCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.ORCID 0000-0002-7954-5753
Sandra Rayego-MateosCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.ORCID 0000-0001-6874-2359
Vanessa MarchantCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.
Raul R Rodrigues-DiezRed de Investigación Renal (REDinREN), Instituto de Salud Carlos III, 28040 Madrid, Spain.ORCID 0000-0002-2456-6709
Irene Rubio-SotoCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.
Sebastiaan N KnoppertDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
Alberto OrtizRed de Investigación Renal (REDinREN), Instituto de Salud Carlos III, 28040 Madrid, Spain.ORCID 0000-0002-9805-9523
Adrian M RamosRed de Investigación Renal (REDinREN), Instituto de Salud Carlos III, 28040 Madrid, Spain.
Roel GoldschmedingDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
Marta Ruiz-OrtegaCellular Biology in Renal Diseases Laboratory, IIS-Fundación Jiménez Díaz, Universidad Autónoma Madrid, 28040 Madrid, Spain.ORCID 0000-0002-1495-6535
Instituto de Salud Carlos III · ESHeidelberg University · DE

Funding

Fundacion Conchita RabagoInnovation programme under the Marie Skłodowska-Curie grant of the European Union's Horizon 2020 IMProve-PD ID: 812699Instituto de Salud Carlos III CD20/00042Instituto de Salud Carlos III DTS20/00083Instituto de Salud Carlos III PI17/00119Instituto de Salud Carlos III PI18/01133Instituto de Salud Carlos III PI20/00140Juan de la Cierva incorporacion IJC2018-035187-IMinistry of Economy, Industry and Competitiveness EIN2019-103294NOVELREN-CM: Enfermedad renal crónica: nuevas Estrategias para la prevención, Diagnóstico y tratamiento B2017/BMD-3751Red de Investigación Renal REDINREN RD16/0009/0003
6 · The paper itself

Abstract

Chronic kidney disease (CKD) can be considered as a clinical model for premature aging. However, non-invasive biomarkers to detect early kidney damage and the onset of a senescent phenotype are lacking. Most of the preclinical senescence studies in aging have been done in very old mice. Furthermore, the precise characterization and over-time development of age-related senescence in the kidney remain unclear. To address these limitations, the age-related activation of cellular senescence-associated mechanisms and their correlation with early structural changes in the kidney were investigated in 3- to 18-month-old C57BL6 mice. Inflammatory cell infiltration was observed by 12 months, whereas tubular damage and collagen accumulation occurred later. Early activation of cellular-senescence-associated mechanisms was found in 12-month-old mice, characterized by activation of the DNA-damage-response (DDR), mainly in tubular cells; activation of the antioxidant NRF2 pathway; and klotho downregulation. However, induction of tubular-cell-cycle-arrest (CCA) and overexpression of renal senescent-associated secretory phenotype (SASP) components was only found in 18-month-old mice. In aging mice, both inflammation and oxidative stress (marked by elevated lipid peroxidation and NRF2 inactivation) remained increased. These findings support the hypothesis that prolonged DDR and CCA, loss of nephroprotective factors (klotho), and dysfunctional redox regulatory mechanisms (NRF2/antioxidant defense) can be early drivers of age-related kidney-damage progression.

Indexed as

aging kidneycellular senescencefibrosisinflammagingNRF2oxidation

Identifiers

PMID35204184
PMCPMC8868560
OpenAlexW4210452950

What OpenQuestion holds

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Registered trials

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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.