Evidence map›Paper›PMID 31117242›Full record

ArticleInternational journal of molecular sciences2019

MST1 Regulates Neuronal Cell Death via JNK/Casp3 Signaling Pathway in HFD Mouse Brain and HT22 Cells.

Mehtab Khan, Bart P F Rutten, Myeong Ok Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. 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
3.0field-weighted citation impact, top 9% 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, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025
    Review
  7. Article
  8. Article
  9. Effect of insulin on IR and GLP1-R expressions in HT22 cells.Medical oncology (Northwood, London, England) · 2023
    Article
  10. OncogenicNeural regeneration research · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
  16. Article
  17. Review
  18. Article
  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

3 authors at 2 institutions in 2 countries.

Mehtab KhanDivision of Life Science and Applied Life Science (BK21 Plus), College of Natural Sciences, Gyeongsang National University, Jinju 52828, Korea. mehtabneuro@gnu.ac.kr.
Bart P F RuttenDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Faculty of Health, Medicine and Life Sciences, Maastricht University, European Graduate School of Neuroscience (EURON), Maastricht, The Netherlands. b.rutten@maastrichtuniversity.nl.
Myeong Ok KimDivision of Life Science and Applied Life Science (BK21 Plus), College of Natural Sciences, Gyeongsang National University, Jinju 52828, Korea. mokim@gnu.ac.kr.
Gyeongsang National University · KRMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress has been considered as the main mediator in neurodegenerative diseases. A high-fat diet (HFD) and metabolic diseases result in oxidative stress generation, leading to various neurodegenerative diseases via molecular mechanisms that remain largely unknown. Protein kinases play an important role in the homeostasis between cell survival and cell apoptosis. The mammalian sterile 20-like kinase-1 (MST1) protein kinase plays an important role in cellular apoptosis in different organ systems, including the central nervous system. In this study, we evaluated the MST1/c-Jun N-terminal kinase (JNK) dependent oxidative damage mediated cognitive dysfunction in HFD-fed mice and stress-induced hippocampal HT22 (mice hippocampal) cells. Our Western blot and immunofluorescence results indicate that HFD and stress-induced hippocampal HT22 cells activate MST1/JNK/Caspase-3 (Casp-3) signaling, which regulates neuronal cell apoptosis and beta-amyloid-cleaving enzyme (BACE1) expression and leads to impaired cognition. Moreover, MST1 expression inhibition by shRNA significantly reduced JNK/Casp-3 signaling. Our in vivo and in vitro experiments mimicking metabolic stress, such as a high-fat diet, hyperglycemia, and an inflammatory response, determined that MST1 plays a key regulatory role in neuronal cell death and cognition, suggesting that MST1 could be a potential therapeutic target for numerous neurodegenerative diseases.

Indexed as

ApoptosisDiet, High-FatSignal TransductionAnimalsBrainCaspase 3Cell LineHippo KinasesJNK Mitogen-Activated Protein KinasesMaleMiceMice, Inbred C57BLProtein Serine-Threonine KinasesCaspase 3Hippo KinasesJNK Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesStk4 protein, mouseapoptosishigh-fat dietJNKMST1neurodegenerationROS

Identifiers

PMID31117242
PMCPMC6566356
OpenAlexW2944873817

What OpenQuestion holds

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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.