Evidence map›Paper›PMID 28381463›Full record

ArticleAmerican journal of physiology. Renal physiology2017

Chronic kidney disease induces autophagy leading to dysfunction of mitochondria in skeletal muscle.

Zhen Su, Janet D Klein, Jie Du, Harold A Franch, Liping Zhang, Faten Hassounah, Matthew B Hudson, Xiaonan H Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
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  9. Observational
  10. Article
  11. Targeting Sarcopenia in CKD: The Emerging Role of GLP-1 Receptor Agonists.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Review
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  17. Review
  18. Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023
    Review
  19. Article
  20. Article
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

8 authors at 5 institutions in 2 countries.

Zhen SuDepartment of Nephrology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Janet D KleinRenal Division, Department of Medicine, Emory University, Atlanta, Georgia.
Jie DuThe Key Laboratory of Remodeling-related Cardiovascular Diseases, Beijing Anzhen Hospital Affiliated with Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China.
Harold A FranchRenal Division, Department of Medicine, Emory University, Atlanta, Georgia.
Liping ZhangNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, Texas; and.
Faten HassounahRenal Division, Department of Medicine, Emory University, Atlanta, Georgia.
Matthew B HudsonDepartment of Kinesiology, Temple University, Philadelphia, Pennsylvania.
Xiaonan H WangRenal Division, Department of Medicine, Emory University, Atlanta, Georgia xwang03@emory.edu.
Emory University · USBaylor College of Medicine · USBeijing Anzhen Hospital · CNTemple University · USWenzhou Medical University · CN

Funding

MicroRNA and Muscle Wasting in UremiaR01AR060268 · NIAMS · EMORY UNIVERSITY · PI WANG, XIAONAN H · 2012 to 2016
$1.7M
NIAMS NIH HHS R01 AR060268
6 · The paper itself

Abstract

Chronic kidney disease (CKD) causes loss of lean body mass by multiple mechanisms. This study examines whether autophagy-mediated proteolysis contributes to CKD-induced muscle wasting. We tested autophagy in the muscle of CKD mice with plantaris muscle overloading to mimic resistance exercise or with acupuncture plus low-frequency electrical stimulation (Acu/LFES) treatment. In CKD muscle, Bnip3, Beclin-1, and LC3II mRNAs and proteins were increased compared with those in control muscle, indicating autophagosome-lysosome formation induction. Acu/LFES suppressed the CKD-induced upregulation of autophagy. However, overloading increased autophagy-related proteins in normal and CKD muscle. Serum from uremic mice induces autophagy formation but did not increase the myosin degradation or actin break down in cultured muscle satellite cells. We examined mitochondrial biogenesis, copy number, and ATP production in cultured myotubes, and found all three aspects to be decreased by uremic serum. Inhibition of autophagy partially reversed this decline in cultured myotubes. In CKD mice, the mitochondrial copy number, biogenesis marker peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial transcription factor A (TFAM), and mitochondrial fusion marker Mitofusin-2 (Mfn2) are decreased. Both muscle overloading and Acu/LFES increased mitochondrial copy number, and reversed the CKD-induced decreases in PGC-1α, TFAM, and Mfn2. We conclude that the autophagy is activated in the muscle of CKD mice. However, myofibrillar protein is not directly broken down through autophagy. Instead, CKD-induced upregulation of autophagy leads to dysfunction of mitochondria and decrease of ATP production.

Indexed as

AutophagyAdenosine TriphosphateAnimalsBeclin-1Cell LineDisease Models, AnimalDNA-Binding ProteinsGene Expression RegulationGTP PhosphohydrolasesHigh Mobility Group ProteinsMaleMembrane ProteinsMiceMice, Inbred C57BLMicrotubule-Associated ProteinsMitochondrial ProteinsAdenosine TriphosphateBeclin-1Becn1 protein, mouseBNip3 protein, mouseDNA-Binding ProteinsGTP PhosphohydrolasesHigh Mobility Group ProteinsMap1lc3b protein, mouseMembrane ProteinsMFN2 protein, humanMicrotubule-Associated ProteinsMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseRNA, MessengerTfam protein, mouseacidificationforkhead transcription factorsFoxOLC3IIoverloadingubiquitin-proteasome system

Identifiers

PMID28381463
PMCPMC5495886
OpenAlexW2604787319

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.