Evidence map›Paper›PMID 34439810›Full record

ReviewBiomolecules2021

Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases.

Ana Karina Aranda-Rivera, Alfredo Cruz-Gregorio, Omar Emiliano Aparicio-Trejo, José Pedraza-Chaverri

Abstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
–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

123 citing papers in PubMed.

  1. Review
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  14. HACS omega · 2026
    Article
  15. Review
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  18. Review
  19. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026
    Review
  20. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

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
Alfredo Cruz-GregorioLaboratorio F-225, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0003-0077-5079
Omar Emiliano Aparicio-TrejoDepartmento de Fisiopatología Cardio-Renal, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City 14080, Mexico.ORCID 0000-0002-7701-4537
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

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

Indexed as

Oxidative StressProtein Processing, Post-TranslationalAcute Kidney InjuryApoptosisFatty AcidsHumansKidneyMitochondriaMitochondrial DynamicsMitophagyNADPH Oxidase 1NF-kappa BOxidative PhosphorylationReactive Oxygen SpeciesRenal Insufficiency, ChronicSignal TransductionFatty AcidsNADPH Oxidase 1NF-kappa BNOX1 protein, humanReactive Oxygen SpeciesSuperoxide Dismutaseacute kidney injury (AKI)biogenesischronic kidney disease (CKD)fatty acid (FA) β-oxidationmitochondrial dynamicsmitochondrial metabolismmitochondrial proteinsmitochondrial redox signalingmitophagyoxidative phosphorylation (OXPHOS)tricarboxylic acid (TCA) cycle

Identifiers

PMID34439810
PMCPMC8391472

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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.