Evidence map›Paper›PMID 32987643›Full record

ArticleMolecules (Basel, Switzerland)2020

Treatment with Mammalian Ste-20-like Kinase 1/2 (MST1/2) Inhibitor XMU-MP-1 Improves Glucose Tolerance in Streptozotocin-Induced Diabetes Mice.

Zakiyatul Faizah, Bella Amanda, Faisal Yusuf Ashari, Efta Triastuti, Rebecca Oxtoby, Anny Setijo Rahaju, M Aminudin Aziz, Maria Inge Lusida, Delvac Oceandy

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Apoptosis in Type 2 Diabetes: Can It Be Prevented? Hippo Pathway Prospects.International journal of molecular sciences · 2022
    Review
  10. 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

9 authors at 3 institutions in 2 countries.

Zakiyatul FaizahDepartment of Biomedical Sciences, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
Bella AmandaDepartment of Biomedical Sciences, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
Faisal Yusuf AshariDepartment of Biomedical Sciences, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
Efta TriastutiDivision of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK.
Rebecca OxtobyDivision of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK.
Anny Setijo RahajuDepartment of Anatomical Pathology, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
M Aminudin AzizDepartment of Biomedical Sciences, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
Maria Inge LusidaInstitute of Tropical Disease, Universitas Airlangga, Surabaya 60286, Indonesia.
Delvac OceandyDivision of Cardiovascular Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PT, UK.
Airlangga University · IDUniversity of Manchester · GBUniversity of Brawijaya · ID

Funding

British Heart Foundation PG/17/78/33304British Heart Foundation PG/18/40/33767Universitas Airlangga 1408/UN3/2019
6 · The paper itself

Abstract

Diabetes mellitus (DM) is one of the major causes of death in the world. There are two types of DM-type 1 DM and type 2 DM. Type 1 DM can only be treated by insulin injection whereas type 2 DM is commonly treated using anti-hyperglycemic agents. Despite its effectiveness in controlling blood glucose level, this therapeutic approach is not able to reduce the decline in the number of functional pancreatic β cells. MST1 is a strong pro-apoptotic kinase that is expressed in pancreatic β cells. It induces β cell death and impairs insulin secretion. Recently, a potent and specific inhibitor for MST1, called XMU-MP-1, was identified and characterized. We hypothesized that treatment with XMU-MP-1 would produce beneficial effects by improving the survival and function of the pancreatic β cells. We used INS-1 cells and STZ-induced diabetic mice as in vitro and in vivo models to test the effect of XMU-MP-1 treatment. We found that XMU-MP-1 inhibited MST1/2 activity in INS-1 cells. Moreover, treatment with XMU-MP-1 produced a beneficial effect in improving glucose tolerance in the STZ-induced diabetic mouse model. Histological analysis indicated that XMU-MP-1 increased the number of pancreatic β cells and enhanced Langerhans islet area in the severe diabetic mice. Overall, this study showed that MST1 could become a promising therapeutic target for diabetes mellitus.

Indexed as

AnimalsBenzenesulfonamidesCell LineDiabetes Mellitus, ExperimentalGlucose IntoleranceHippo KinasesInsulin-Secreting CellsMaleMiceMice, Inbred BALB CProtein Serine-Threonine KinasesSerine-Threonine Kinase 3SulfonamidesBenzenesulfonamidesHippo KinasesProtein Serine-Threonine KinasesSerine-Threonine Kinase 3Stk3 protein, mouseStk4 protein, mouseSulfonamidesXMU-MP-1diabetes mellitusHippo pathwayMST1/2XMU-MP-1

Identifiers

PMID32987643
PMCPMC7582334
OpenAlexW3088022081

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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.