Evidence map›Paper›PMID 33235391›Full record

ReviewNature reviews. Nephrology2021

Mitochondrial quality control in kidney injury and repair.

Chengyuan Tang, Juan Cai, Xiao-Ming Yin, Joel M Weinberg, Manjeri A Venkatachalam, Zheng Dong

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 284 papers.

0numbers the graph read from it
0cells of the map it votes in
284citing papers in PubMed
28.7field-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

284 citing papers in PubMed, 480 citations in OpenAlex.

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  17. Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
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224 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

6 authors at 4 institutions in 2 countries.

Chengyuan TangDepartment of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital at Central South University, Changsha, China.ORCID http://orcid.org/0000-0001-9522-4469
Juan CaiDepartment of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital at Central South University, Changsha, China.
Xiao-Ming YinDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
Joel M WeinbergDepartment of Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Manjeri A VenkatachalamDepartment of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Zheng DongDepartment of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital at Central South University, Changsha, China. zdong@augusta.edu.ORCID http://orcid.org/0000-0003-3538-8095
Central South University · CNIndiana University School of MedicineThe University of Texas Health Science Center at San Antonio · USUniversity of Michigan · US

Funding

Pathogenesis of tubule atrophy and failed recovery after acute kidney injuryR01DK104128 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI VENKATACHALAM, MANJERI A · 2016 to 2019
$1.4M
Mitochondrial Recovery after Acute Kidney Injury Needs Ribonucleotide ReductaseR01DK119693 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI VENKATACHALAM, MANJERI A · 2020 to 2022
$696k
NIDDK NIH HHS R01 DK104128NIDDK NIH HHS R01 DK119693
6 · The paper itself

Abstract

Mitochondria are essential for the activity, function and viability of eukaryotic cells and mitochondrial dysfunction is involved in the pathogenesis of acute kidney injury (AKI) and chronic kidney disease, as well as in abnormal kidney repair after AKI. Multiple quality control mechanisms, including antioxidant defence, protein quality control, mitochondrial DNA repair, mitochondrial dynamics, mitophagy and mitochondrial biogenesis, have evolved to preserve mitochondrial homeostasis under physiological and pathological conditions. Loss of these mechanisms may induce mitochondrial damage and dysfunction, leading to cell death, tissue injury and, potentially, organ failure. Accumulating evidence suggests a role of disturbances in mitochondrial quality control in the pathogenesis of AKI, incomplete or maladaptive kidney repair and chronic kidney disease. Moreover, specific interventions that target mitochondrial quality control mechanisms to preserve and restore mitochondrial function have emerged as promising therapeutic strategies to prevent and treat kidney injury and accelerate kidney repair. However, clinical translation of these findings is challenging owing to potential adverse effects, unclear mechanisms of action and a lack of knowledge of the specific roles and regulation of mitochondrial quality control mechanisms in kidney resident and circulating cell types during injury and repair of the kidney.

Indexed as

Acute Kidney InjuryAnimalsHumansMitochondriaRenal Insufficiency, Chronic

Identifiers

PMID33235391
PMCPMC8958893
OpenAlexW3110011931

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.