Evidence map›Paper›PMID 32868492›Full record

ReviewKidney research and clinical practice2020

Mitochondrial dysfunction in kidney injury, inflammation, and disease: Potential therapeutic approaches.

Divya Bhatia, Allyson Capili, Mary E Choi

Open access · diamondAbstract readReview
In one paragraph

Review in Kidney research and clinical practice, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 2 pooled it
8.5field-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

118 citing papers in PubMed, 2 syntheses or guidelines pooled it, 180 citations in OpenAlex.

  1. Pooled it
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  12. Sex determines cardiac and renal Vulnerability to chronic hemoglobin toxicity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Article
  13. Article
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  17. Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  19. Article
  20. Review

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

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

3 authors at 1 institution in 1 country.

Divya BhatiaDivision of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.ORCID https://orcid.org/0000-0002-8236-3440
Allyson CapiliDivision of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.ORCID https://orcid.org/0000-0003-0557-273X
Mary E ChoiDivision of Nephrology and Hypertension, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.ORCID https://orcid.org/0000-0002-6853-336X
NewYork–Presbyterian Hospital · US

Funding

The Role of HEME Oxygenase in Hyperoxic Lung InjuryR01HL055330 · NHLBI · YALE UNIVERSITY · PI CHOI, AUGUSTINE M, CHOI, MARY E · 1998 to 2021
$6.6M
Metabolic dysfunction regulates mitophagy-dependent necroptosis in COPDR01HL132198 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, AUGUSTINE M, CHOI, MARY E · 2017 to 2020
$2.2M
Novel role of RIPK3-dependent necroptosis pathway in lung and kidney fibrosisR01HL133801 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, AUGUSTINE M, CHOI, MARY E · 2017 to 2020
$2.1M
NHLBI NIH HHS R01 HL055330NHLBI NIH HHS R01 HL132198NHLBI NIH HHS R01 HL133801
6 · The paper itself

Abstract

Mitochondria are energy-producing organelles that not only satisfy the high metabolic demands of the kidney but sense and respond to kidney injury-induced oxidative stress and inflammation. Kidneys are rich in mitochondria. Mitochondrial dysfunction plays a critical role in the progression of acute kidney injury and chronic kidney disease. Mitochondrial responses to specific stimuli are highly regulated and synergistically modulated by tightly interconnected processes, including mitochondrial dynamics (fission, fusion) and mitophagy. The counterbalance between these processes is essential in maintaining a healthy network of mitochondria. Recent literature suggests that alterations in mitochondrial dynamics are implicated in kidney injury and the progression of kidney diseases. A decrease in mitochondrial fusion promotes fission-induced mitochondrial fragmentation, but a reduction in mitochondrial fission produces excessive mitochondrial elongation. The removal of dysfunctional mitochondria by mitophagy is crucial for their quality control. Defective mitochondrial function disrupts cellular redox potential and can cause cell death. Mitochondrial DNA derived from damaged cells also act as damage-associated molecular patterns to recruit immune cells and the inflammatory response can further exaggerate kidney injury. This review provides a comprehensive overview of the role of mitochondrial dysfunction in acute kidney injury and chronic kidney disease. We discuss the processes that control mitochondrial stress responses to kidney injury and review recent advances in understanding the role of mitochondrial dysfunction in inflammation and tissue damage through the use of different experimental models of kidney disease. We also describe potential mitochondria-targeted therapeutic approaches.

Indexed as

Acute kidney injuryInflammationKidney diseasesMitochondriaOxidative stress

Identifiers

PMID32868492
PMCPMC7530368
OpenAlexW3082090275

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.