Evidence map›Paper›PMID 29391924›Full record

ReviewOxidative medicine and cellular longevity2017

How AMPK and PKA Interplay to Regulate Mitochondrial Function and Survival in Models of Ischemia and Diabetes.

Jingdian Zhang, Yumeng Wang, Xiaofeng Liu, Ruben K Dagda, Ying Zhang

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Adenosine A2A receptor activation reduces chondrocyte senescence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Ketamine plus Alcohol: What We Know and What We Can Expect about This.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors at 3 institutions in 2 countries.

Jingdian ZhangDepartment of Neurology and Neuroscience Center, First Hospital of Jilin University, Xinmin Street No. 71, Changchun 130000, China.ORCID 0000-0002-5685-8386
Yumeng WangDepartment of Physiology, College of Basic Medical Sciences, Norman Bethune Health Science Center, Jilin University, Xinmin Street No. 126, Changchun 130000, China.ORCID 0000-0001-5863-0425
Xiaofeng LiuNeuroscience Research Center, The First Hospital of Jilin University, East Democracy Street No. 519, Changchun 130000, China.ORCID 0000-0001-6626-1906
Ruben K DagdaDepartment of Pharmacology, University of Nevada, Reno School of Medicine, Mailstop 318, Manville Health Sciences Building 19A(Office)/18, Reno, NV 89557, USA.ORCID 0000-0002-9946-9591
Ying ZhangDepartment of Neurology and Neuroscience Center, First Hospital of Jilin University, Xinmin Street No. 71, Changchun 130000, China.ORCID 0000-0002-4448-2051
Jilin University · CNFirst Bethune Hospital of Jilin University · CNUniversity of Nevada, Reno · US

Funding

Cell Biology of Signaling across MembranesP20GM103554 · NIGMS · UNIVERSITY OF NEVADA RENO · PI VON BARTHELD, CHRISTOPHER S · 2012 to 2016
$8.0M
NIGMS NIH HHS P20 GM103554
6 · The paper itself

Abstract

Adenosine monophosphate-activated protein kinase (AMPK) is a conserved, redox-activated master regulator of cell metabolism. In the presence of oxidative stress, AMPK promotes cytoprotection by enhancing the conservation of energy by suppressing protein translation and by stimulating autophagy. AMPK interplays with protein kinase A (PKA) to regulate oxidative stress, mitochondrial function, and cell survival. AMPK and dual-specificity A-kinase anchoring protein 1 (D-AKAP1), a mitochondrial-directed scaffold of PKA, interact to regulate mitochondrial function and oxidative stress in cardiac and endothelial cells. Ischemia and diabetes, a chronic disease that increases the onset of cardiovascular diseases, suppress the cardioprotective effects of AMPK and PKA. Here, we review the molecular mechanisms by which AMPK and D-AKAP1/PKA interplay to regulate mitochondrial function, oxidative stress, and signaling pathways that prime endothelial cells, cardiac cells, and neurons for cytoprotection against oxidative stress. We discuss recent literature showing how temporal dynamics and localization of activated AMPK and PKA holoenzymes play a crucial role in governing cellular bioenergetics and cell survival in models of ischemia, cardiovascular diseases, and diabetes. Finally, we propose therapeutic strategies that tout localized PKA and AMPK signaling to reverse mitochondrial dysfunction, oxidative stress, and death of neurons and cardiac and endothelial cells during ischemia and diabetes.

Indexed as

AMP-Activated Protein KinasesCyclic AMP-Dependent Protein KinasesDiabetes MellitusHumansIschemiaMitochondriaSurvival AnalysisAMP-Activated Protein KinasesCyclic AMP-Dependent Protein Kinases

Identifiers

PMID29391924
PMCPMC5748092
OpenAlexW2774435753

What Socratic 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 Socratic graph.