Evidence map›Paper›PMID 29884802›Full record

ArticleScientific reports2018

Chloroquine and amodiaquine enhance AMPK phosphorylation and improve mitochondrial fragmentation in diabetic tubulopathy.

Hye Yun Jeong, Jun Mo Kang, Hak Hoon Jun, Dong-Jin Kim, Seon Hwa Park, Min Ji Sung, Jin Hyung Heo, Dong Ho Yang, Sang Ho Lee, So-Young Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Critical Role for AMPK in Metabolic Disease-Induced Chronic Kidney Disease.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Cardiac effects and toxicity of chloroquine: a short update.International journal of antimicrobial agents · 2020
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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

10 authors at 3 institutions in 1 country.

Hye Yun JeongDivision of Nephrology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Jun Mo KangDivision of Nephrology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Hak Hoon JunDepartment of Surgery, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Dong-Jin KimDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Kyung Hee University, Seoul, South Korea.
Seon Hwa ParkDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Kyung Hee University, Seoul, South Korea.
Min Ji SungDivision of Nephrology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Jin Hyung HeoDepartment of Pathology, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Dong Ho YangDivision of Nephrology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea.
Sang Ho LeeDivision of Nephrology, Department of Internal Medicine, Kyung Hee University Hospital at Gangdong, Kyung Hee University, Seoul, South Korea. lshkidney@khu.ac.kr.
So-Young LeeDivision of Nephrology, Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, South Korea. ysy0119@cha.ac.kr.
CHA University · KRCHA University Bundang Medical Center · KRKyung Hee University Hospital at Gangdong · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the effects of chloroquine (CQ) and amodiaquine (AQ) on AMPK phosphorylation in renal tubular cells in a diabetic environment in vivo and in vitro. We also examined whether CQ- or AQ-mediated AMPK activity restoration attenuated diabetic tubulopathy by normalizing mitochondrial fragmentation. Human renal proximal epithelial cells (HKC8) were incubated in high-glucose conditions. Diabetes was induced with streptozotocin in male C57/BL6J mice. Treatment with CQ or AQ abolished high-glucose-induced phospho-AMPK and phosph-PGC1α down-regulation in HKC8 cells. Improvements in functional mitochondrial mass and balanced fusion/fission protein expression were observed in HKC8 cells after treatment with CQ or AQ in high-glucose conditions. Moreover, decreased mitochondrial ROS production and reduced apoptotic and fibrotic protein expression were noted in HKC8 cells after treatment with CQ or AQ, even in high-glucose conditions. CQ and AQ treatment effectively mitigated albuminuria and renal histopathologic changes and increased AMPK activity in the kidneys of diabetic mice. Electron microscopy analysis showed that mitochondrial fragmentation was decreased, and 8-OHdG content was low in the renal tubular cells of the CQ and AQ treatment groups compared with those of the diabetic control group. Our results suggest that CQ and AQ may be useful treatments for patients with diabetic kidney disease.

Indexed as

AmodiaquineAMP-Activated Protein KinasesAnimalsAntimalarialsCell LineChloroquineDiabetes Mellitus, ExperimentalDiabetic NephropathiesEnzyme ActivatorsGlucoseHumansKidney TubulesMaleMice, Inbred C57BLMitochondriaPhosphorylationAmodiaquineAMP-Activated Protein KinasesAntimalarialsChloroquineEnzyme ActivatorsGlucose

Identifiers

PMID29884802
PMCPMC5993726
OpenAlexW2807559868

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.