Evidence map›Paper›PMID 34501442›Full record

ReviewJournal of clinical medicine2021

Targeting Mitochondria and Metabolism in Acute Kidney Injury.

Ying Li, Mark Hepokoski, Wanjun Gu, Tatum Simonson, Prabhleen Singh

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.4field-weighted citation impact, top 2% 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, 53 citations in OpenAlex.

  1. Article
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  16. Review
  17. Review
  18. Metabolic mechanisms of acute proximal tubular injury.Pflugers Archiv : European journal of physiology · 2022
    Review
  19. Article
  20. Organelle Stress and Metabolic Derangement in Kidney Disease.International journal of molecular sciences · 2022
    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

5 authors at 3 institutions in 1 country.

Ying LiDivision of Nephrology and Hypertension, University of California San Diego, San Diego, CA 92093, USA.
Mark HepokoskiVA San Diego Healthcare System, San Diego, CA 92161, USA.
Wanjun GuDivision of Pulmonary, Critical Care and Sleep Medicine, University of California San Diego, San Diego, CA 92093, USA.
Tatum SimonsonDivision of Pulmonary, Critical Care and Sleep Medicine, University of California San Diego, San Diego, CA 92093, USA.
Prabhleen SinghDivision of Nephrology and Hypertension, University of California San Diego, San Diego, CA 92093, USA.
University of California, San Diego · USUniversity of California System · USVA San Diego Healthcare System · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CURTIS, LISA M · 2008 to 2022
$18.3M
Respiratory and genomic contributions to adaptive/maladaptive hypoxia responsesR01HL145470 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SIMONSON, TATUM S · 2019 to 2023
$2.4M
Renal Oxygenation and Mitochondrial Function in AKIR01DK107852 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SINGH, PRABHLEEN · 2016 to 2020
$1.7M
Renal Oxygenation in the Pathophysiology of Kidney DiseaseI01BX002175 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI SINGH, PRABHLEEN · 2015 to 2025
–
BLRD VA I01 BX002175BLRD VA IK2 BX004338NHLBI NIH HHS R01 HL145470NIDDK NIH HHS P30 DK079337NIDDK NIH HHS P30DK079337NIDDK NIH HHS R01 DK107852NIDDK NIH HHS R01DK107852
6 · The paper itself

Abstract

Acute kidney injury (AKI) significantly contributes to morbidity and mortality in critically ill patients. AKI is also an independent risk factor for the development and progression of chronic kidney disease. Effective therapeutic strategies for AKI are limited, but emerging evidence indicates a prominent role of mitochondrial dysfunction and altered tubular metabolism in the pathogenesis of AKI. Therefore, a comprehensive, mechanistic understanding of mitochondrial function and renal metabolism in AKI may lead to the development of novel therapies in AKI. In this review, we provide an overview of current state of research on the role of mitochondria and tubular metabolism in AKI from both pre-clinical and clinical studies. We also highlight current therapeutic strategies which target mitochondrial function and metabolic pathways for the treatment of AKI.

Indexed as

energy metabolismkidney injurymitochondria

Identifiers

PMID34501442
PMCPMC8432487
OpenAlexW3197207873

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.