Evidence map›Paper›PMID 32538150›Full record

ArticleAmerican journal of physiology. Renal physiology2020

Evolution of altered tubular metabolism and mitochondrial function in sepsis-associated acute kidney injury.

Ying Li, Noureddin Nourbakhsh, Hai Pham, Rick Tham, Jonathan E Zuckerman, Prabhleen Singh

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  11. Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025
    Review
  12. Review
  13. Assays to enhance metabolic phenotyping in the kidney.American journal of physiology. Renal physiology · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Ying LiDivision of Nephrology-Hypertension, University of California, San Diego, California.
Noureddin NourbakhshDivision of Nephrology-Hypertension, University of California, San Diego, California.
Hai PhamDivision of Nephrology-Hypertension, University of California, San Diego, California.
Rick ThamDivision of Nephrology-Hypertension, University of California, San Diego, California.
Jonathan E ZuckermanDepartment of Pathology and Laboratory Medicine, University of California, Los Angeles, California.
Prabhleen SinghDivision of Nephrology-Hypertension, University of California, San Diego, California.ORCID 0000-0001-5555-261X
University of California San Diego · USUniversity of California, Los Angeles · 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
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 BX002175HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) P30-DK 079337NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK107852
6 · The paper itself

Abstract

Sepsis-associated acute kidney injury (s-AKI) has a staggering impact in patients and lacks any treatment. Incomplete understanding of the pathogenesis of s-AKI is a major barrier to the development of effective therapies. We address the gaps in knowledge regarding renal oxygenation, tubular metabolism, and mitochondrial function in the pathogenesis of s-AKI using the cecal ligation and puncture (CLP) model in mice. At 24 h after CLP, renal oxygen delivery was reduced; however, fractional oxygen extraction was unchanged, suggesting inefficient renal oxygen utilization despite decreased glomerular filtration rate and filtered load. To investigate the underlying mechanisms, we examined temporal changes in mitochondrial function and metabolism at 4 and 24 h after CLP. At 4 h after CLP, markers of mitochondrial content and biogenesis were increased in CLP kidneys, but mitochondrial oxygen consumption rates were suppressed in proximal tubules. Interestingly, at 24 h, proximal tubular mitochondria displayed high respiratory capacity, but with decreased mitochondrial content, biogenesis, fusion, and ATP levels in CLP kidneys, suggesting decreased ATP synthesis efficiency. We further investigated metabolic reprogramming after CLP and observed reduced expression of fatty acid oxidation enzymes but increased expression of glycolytic enzymes at 24 h. However, assessment of functional glycolysis revealed lower glycolytic capacity, glycolytic reserve, and compensatory glycolysis in CLP proximal tubules, which may explain their susceptibility to injury. In conclusion, we demonstrated significant alterations in renal oxygenation, tubular mitochondrial function, and metabolic reprogramming in s-AKI, which may play an important role in the progression of injury and recovery from AKI in sepsis.

Indexed as

Acute Kidney InjuryAnimalsDisease Models, AnimalKidneyKidney Tubules, ProximalMice, Inbred C57BLMitochondriaSepsisacute kidney injurymetabolismmitochondriaoxygenation

Identifiers

PMID32538150
PMCPMC7473900
OpenAlexW3035235416

What OpenQuestion holds

Textmetadata
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.