Evidence map›Paper›PMID 30338935›Full record

ArticleJournal of cellular and molecular medicine2019

Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis.

Zheng Cheng, Mingming Zhang, Jianqiang Hu, Jie Lin, Xinyu Feng, Shanjie Wang, Tingting Wang, Erhe Gao, Haichang Wang, Dongdong Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. Mammalian STE20-like kinase 1 inhibits synoviocytes activation in rheumatoid arthritis through mitochondrial dysfunction mediated by SIRT3/mTOR axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  8. Review
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  10. Increased ATHypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Hippo Signaling Pathway in Cardiac Development and Diseases.Frontiers in cell and developmental biology · 2019
    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

10 authors at 2 institutions in 2 countries.

Zheng ChengDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Mingming ZhangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Jianqiang HuDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Jie LinDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Xinyu FengDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Shanjie WangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Tingting WangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Erhe GaoCenter for Translational Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania.
Haichang WangDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
Dongdong SunDepartment of Cardiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0003-2147-3977
Xijing Hospital · CNTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is associated with various myocardial diseases. Angiotensin II (Ang II) plays a central role in the pathogenesis of RAAS-triggered cardiac apoptosis. Our previous studies showed that mammalian Ste20-like kinase 1 (Mst1) aggravates cardiac dysfunction in cardiomyocyte under pathological conditions, but its role in Ang II-mediated cardiomyocyte apoptosis is not known. We addressed this in the present study by investigating whether cardiac-specific Mst1 knockout can alleviate Ang II-induced cardiomyocyte apoptosis along with the underlying mechanisms. In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Interestingly, Mst1 knockout failed to alleviate Ang II-induced phosphorylation of extracellular signal-regulated kinase 1/2, and inactivated apoptosis signal-regulating kinase1 (ASK1) by promoting its association with thioredoxin (Trx), which reversed the Ang II-induced activation of the ASK1-JNK pathway and suppressed Ang II-induced cardiomyocyte apoptosis. Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure.

Indexed as

AcetylcysteineAngiotensin IIAnimalsApoptosisCardiomyopathiesHippo KinasesJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Kinase Kinase 5MiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacPhosphorylationProtein Serine-Threonine KinasesReactive Oxygen SpeciesAcetylcysteineAngiotensin IIHippo KinasesJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5Protein Serine-Threonine KinasesReactive Oxygen SpeciesStk4 protein, mouseThioredoxinsAngiotensin IIapoptosisASK1JNKMst1ROSTrx

Identifiers

PMID30338935
PMCPMC6307828
OpenAlexW2896470788

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.