Evidence map›Paper›PMID 31276028›Full record

ArticleMedical research archives2019

Mitochondrial dysfunction in acute kidney injury and sex-specific implications.

Jenny S Pan, David Sheikh-Hamad

Open access · greenAbstract read
In one paragraph

Article in Medical research archives, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Article
  10. The Activation of cGAS-STING in Acute Kidney Injury.Journal of inflammation research · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. αInternational journal of molecular sciences · 2020
    Article
  18. Frailty in Critical Care Medicine: A Review.Anesthesia and analgesia · 2020
    Review
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Jenny S PanSection of Nephrology and Center for Translational Research on Inflammatory Diseases, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA.
David Sheikh-HamadSection of Nephrology and Center for Translational Research on Inflammatory Diseases, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA.
Baylor College of Medicine · US

Funding

Stanniocalcin-1: New paradigms for cytoprotection and anti-inflammationI01BX002006 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI DAVID SHEIKH-HAMAD · 2014 to 2026
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Kidney Protection by AMPKIK2BX002912 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI PAN, JENNY SZU-CHIN · 2017 to 2021
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BLRD VA I01 BX002006BLRD VA IK2 BX002912
6 · The paper itself

Abstract

The kidney is one of the most energy-demanding organs in the human body, and the maintenance of mitochondrial homeostasis is central to kidney function. Recent advances have led to a greater appreciation of how mitochondrial dysfunction contributes to the pathogenesis of AKI, from decreased ATP production, to enhanced mitochondrial oxidative stress, cell necrosis and apoptosis. Accumulating evidence suggests sexual dimorphism in the response to AKI with males demonstrating greater risk for developing ischemia-reperfusion and sepsis-induced kidney injury. In contrast, females may be more susceptible to nephrotoxic-AKI. There are important sex-related differences in mitochondrial respiration, biogenesis and dynamics that likely contribute to the observed sexual dimorphism in AKI. Sex hormones mediate many of these differences with multiple preclinical studies demonstrating the renoprotective actions of estrogen in many rodent models of AKI. Estrogenic control of mitochondrial biogenesis, function and reactive oxygen species (ROS) generation is discussed. Furthermore, the potential role for sex chromosomes in mediating sex differences in AKI is examined. Novel animal models such as the "four core genotypes" (FCG) mouse model provide us with important tools to study sex chromosome effects in kidney health and disease. By understanding the influences of sexual dimorphism or sex hormones on mitochondrial homeostasis and disease manifestations, we may be able to identify novel therapeutic targets and improve existing treatment options for AKI.

Identifiers

PMID31276028
PMCPMC6604647
OpenAlexW2980963701

What OpenQuestion holds

Textmetadata
LicenceTDM
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.