Evidence map›Paper›PMID 28085543›Full record

ArticleAutophagy2017

Deletion of PRKAA triggers mitochondrial fission by inhibiting the autophagy-dependent degradation of DNM1L.

Qilong Wang, Shengnan Wu, Huaiping Zhu, Ye Ding, Xiaoyan Dai, Changhan Ouyang, Young-Min Han, Zhonglin Xie, Ming-Hui Zou

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. [DOT1L controls neuronal amyloid precursor protein expres-sion via the p38 MAPK-mediated mitochondrial dynamics homeostasis axis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Article
  2. Beyond blood flow: the multifaceted role of AMPK in regulating fetal growth at high altitudes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  3. Review
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  5. Article
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  9. Article
  10. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
    Review
  11. Article
  12. Article
  13. NADJournal of lipid and atherosclerosis · 2022
    Review
  14. Oxidative medicine and cellular longevity · 2022
    Article
  15. Review
  16. Review
  17. Article
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  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

9 authors at 1 institution in 1 country.

Qilong Wanga Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Shengnan Wua Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Huaiping Zhua Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Ye Dinga Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Xiaoyan Daia Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Changhan Ouyanga Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Young-Min Hana Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Zhonglin Xiea Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Ming-Hui Zoua Center for Molecular and Translational Medicine, Georgia State University , Atlanta , GA USA.
Georgia State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PRKAA (protein kinase, AMP-activated, α catalytic subunit) regulates mitochondrial biogenesis, function, and turnover. However, the molecular mechanisms by which PRKAA regulates mitochondrial dynamics remain poorly characterized. Here, we report that PRKAA regulated mitochondrial fission via the autophagy-dependent degradation of DNM1L (dynamin 1-like). Deletion of Prkaa1/AMPKα1 or Prkaa2/AMPKα2 resulted in defective autophagy, DNM1L accumulation, and aberrant mitochondrial fragmentation in the mouse aortic endothelium. Furthermore, autophagy inhibition by chloroquine treatment or ATG7 small interfering RNA (siRNA) transfection, upregulated DNM1L expression and triggered DNM1L-mediated mitochondrial fragmentation. In contrast, autophagy activation by overexpression of ATG7 or chronic administration of rapamycin, the MTOR inhibitor, promoted DNM1L degradation and attenuated mitochondrial fragmentation in Prkaa2-deficient (prkaa2

Indexed as

AutophagyGene DeletionMitochondrial DynamicsProteolysisAMP-Activated Protein KinasesAnimalsAortaCell SeparationDynaminsEndothelium, VascularGTP PhosphohydrolasesHumansHuman Umbilical Vein Endothelial CellsMice, Inbred C57BLMicrotubule-Associated ProteinsMitochondrial ProteinsAMP-Activated Protein KinasesDNM1L protein, humanDnm1l protein, mouseDynaminsGTP PhosphohydrolasesMicrotubule-Associated ProteinsMitochondrial ProteinsPhosphoserinePRKAA1 protein, humanPRKAA2 protein, humanSequestosome-1 ProteinSirolimusSQSTM1 protein, humanAMPKautophagyDNM1Lendothelial dysfunctionmitochondrial fissionPRKAA/AMPK catalytic subunit α

Identifiers

PMID28085543
PMCPMC5324848
OpenAlexW2577260066

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.