Evidence mapPaperPMID 37188779Full record

ArticleMolecular psychiatry2023

Targeting PDK2 rescues stress-induced impaired brain energy metabolism.

Changshui Wang, Changmeng Cui, Pengfei Xu, Li Zhu, Hongjia Xue, Beibei Chen, Pei Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.4field-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

18 citing papers in PubMed, 41 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

7 authors at 4 institutions in 2 countries.

Changshui Wang *Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272000, China.ORCID 0000-0001-9968-5115
Changmeng Cui *Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, 272000, China.
Pengfei XuTranslational Pharmaceutical Laboratory, Jining First People's Hospital, Shandong First Medical University, Jining, 272000, China.
Li ZhuTranslational Pharmaceutical Laboratory, Jining First People's Hospital, Shandong First Medical University, Jining, 272000, China.
Hongjia XueFaculty of Science and Engineering, University of Nottingham Ningbo China, Ningbo, 315100, China.
Beibei ChenADFA School of Science, University of New South Wales, Canberra, ACT, Australia.
Pei JiangTranslational Pharmaceutical Laboratory, Jining First People's Hospital, Shandong First Medical University, Jining, 272000, China. jiangpeicsu@sina.com.ORCID 0000-0002-8360-7427
Jining First People's Hospital · CNAffiliated Hospital of Jining Medical University · CNUniversity of Nottingham Ningbo China · CNUNSW Sydney · AU

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81602846National Natural Science Foundation of China (National Science Foundation of China) 82272253Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2021MH145Taishan Scholar Project of Shandong Province tsqn201812159
6 · The paper itself

Abstract

Depression is a mental illness frequently accompanied by disordered energy metabolism. A dysregulated hypothalamus pituitary adrenal axis response with aberrant glucocorticoids (GCs) release is often observed in patients with depression. However, the associated etiology between GCs and brain energy metabolism remains poorly understood. Here, using metabolomic analysis, we showed that the tricarboxylic acid (TCA) cycle was inhibited in chronic social defeat stress (CSDS)-exposed mice and patients with first-episode depression. Decreased mitochondrial oxidative phosphorylation was concomitant with the impairment of the TCA cycle. In parallel, the activity of pyruvate dehydrogenase (PDH), the gatekeeper of mitochondrial TCA flux, was suppressed, which is associated with the CSDS-induced neuronal pyruvate dehydrogenase kinase 2 (PDK2) expression and consequently enhanced PDH phosphorylation. Considering the well-acknowledged role of GCs in energy metabolism, we further demonstrated that glucocorticoid receptors (GR) stimulated PDK2 expression by directly binding to its promoter region. Meanwhile, silencing PDK2 abrogated glucocorticoid-induced PDH inhibition, restored the neuronal oxidative phosphorylation, and improved the flux of isotope-labeled carbon (U-

Indexed as

Energy MetabolismPyruvate Dehydrogenase ComplexAnimalsBrainCitric Acid CycleHumansMicePhosphorylationPyruvate Dehydrogenase Complex

Identifiers

PMID37188779
OpenAlexW4376611459

What Socratic 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 Socratic graph.