Evidence map›Paper›PMID 33681190›Full record

ArticleFrontiers in cell and developmental biology2021

KCa3.1 Mediates Dysregulation of Mitochondrial Quality Control in Diabetic Kidney Disease.

Chunling Huang, Hao Yi, Ying Shi, Qinghua Cao, Yin Shi, Delfine Cheng, Filip Braet, Xin-Ming Chen, Carol A Pollock

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Chunling HuangKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
Hao YiKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
Ying ShiDivision of Nephrology, School of Medicine, Stanford University, Stanford, CA, United States.
Qinghua CaoKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
Yin ShiKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
Delfine ChengDiscipline of Anatomy and Histology, School of Medical Sciences, Faculty of Medicine and Health, The Bosch Institute, University of Sydney, Sydney, NSW, Australia.
Filip BraetDiscipline of Anatomy and Histology, School of Medical Sciences, Faculty of Medicine and Health, The Bosch Institute, University of Sydney, Sydney, NSW, Australia.
Xin-Ming ChenKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
Carol A PollockKolling Institute, Sydney Medical School Northern, Faculty of Medicine and Health, University of Sydney, Royal North Shore Hospital, Sydney, NSW, Australia.
University of Sydney · AURoyal North Shore Hospital · AUStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is implicated in the pathogenesis of diabetic kidney disease. Mitochondrial quality control is primarily mediated by mitochondrial turnover and repair through mitochondrial fission/fusion and mitophagy. We have previously shown that blockade of the calcium-activated potassium channel KCa3.1 ameliorates diabetic renal fibrosis. However, the mechanistic link between KCa3.1 and mitochondrial quality control in diabetic kidney disease is not yet known. Transforming growth factor β1 (TGF-β1) plays a central role in diabetic kidney disease. Recent studies indicate an emerging role of TGF-β1 in the regulation of mitochondrial function. However, the molecular mechanism mediating mitochondrial quality control in response to TGF-β1 remains limited. In this study, mitochondrial function was assessed in TGF-β1-exposed renal proximal tubular epithelial cells (HK2 cells) transfected with scrambled siRNA or KCa3.1 siRNA.

Indexed as

diabetic kidney diseaseKCa3.1mitochondrial dynamicsmitochondrial quality controlmitophagytransforming growth factor β1

Identifiers

PMID33681190
PMCPMC7933228
OpenAlexW3129470144

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.