Evidence map›Paper›PMID 29943223›Full record

ArticleEndocrine2018

Inhibition of endoplasmic reticulum stress by intermedin1-53 attenuates angiotensin II-induced abdominal aortic aneurysm in ApoE KO Mice.

Xian-Qiang Ni, Wei-Wei Lu, Jin-Sheng Zhang, Qing Zhu, Jin-Ling Ren, Yan-Rong Yu, Xiu-Ying Liu, Xiu-Jie Wang, Mei Han, Qing Jing and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Endoplasmic reticulum stress in abdominal aortic aneurysm.International journal of cardiology. Heart & vasculature · 2024
    Review
  3. Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023
    Review
  4. Article
  5. Activating transcription factor 4 aggravates angiotensin II-induced cell dysfunction in human vascular aortic smooth muscle cells via transcriptionally activating fibroblast growth factor 21.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. IntermedinCell death & disease · 2021
    Article
  11. Article
  12. Berberine Reduces AβFrontiers in pharmacology · 2021
    Article
  13. Article
  14. IntermedinAging · 2020
    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

13 authors.

Xian-Qiang NiLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China.
Wei-Wei LuLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China.
Jin-Sheng ZhangLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China.
Qing ZhuLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China.
Jin-Ling RenLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China.
Yan-Rong YuDepartment of Microbiology and Parasitology, School of Basic Medical Science, Peking University, 100083, Beijing, China.
Xiu-Ying LiuKey Laboratory of Genetic Network Biology, Collaborative Innovation Center of Genetics and Development, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Xiu-Jie WangKey Laboratory of Genetic Network Biology, Collaborative Innovation Center of Genetics and Development, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Mei HanDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Key Laboratory of Medical Biotechnology of Hebei Province, Hebei Medical University, 050017, Shijiazhuang, China.
Qing JingKey Laboratory of Stem Cell Biology, Shanghai Institutes for Biological Science, Chinese Academy of Science, Shanghai, China.
Jie DuKey Laboratory of Remodeling-Related Cardiovascular Diseases, Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing An Zhen Hospital, Ministry of Education, Capital Medical University, 100029, Beijing, China.
Chao-Shu TangKey Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University Health Science Center, 100083, Beijing, China.
Yong-Fen QiLaboratory of Cardiovascular Bioactive Molecule, School of Basic Medical Sciences, Peking University, 100083, Beijing, China. yongfenqi@163.com.

Funding

the Collaborative Innovation Center for Cardiovascular Disorders PXM2013_014226_07_000088the Major Research Plan of the National Natural Science Foundation of China for "Regulation Mechanism of Vascular Homeostasis and Remodeling" No. 91339203 to YF Qithe National Natural Science Foundation of China No. 81670434 and 81270407 to YF Qithe National Natural Science Foundation of China No. 91739301
6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS) is involved in the development of abdominal aortic aneurysm (AAA). Since bioactive peptide intermedin (IMD)1-53 protects against AAA formation, here we investigated whether IMD1-53 attenuates AAA by inhibiting ERS. AAA model was induced by angiotensin II (AngII) in ApoE KO mouse background. AngII-treated mouse aortas showed increased ERS gene transcription of caspase12, eukaryotic translation initiation factor 2a (eIf2a) and activating transcription factor 4(ATF4).The protein level of ERS marker glucose regulated protein 94(GRP94), ATF4 and C/EBP homologous protein 10(CHOP) was also up-regulated by AngII. Increased ERS levels were accompanied by severe VSMC apoptosis in human AAA aorta. In vivo administration of IMD1-53 greatly reduced AngII-induced AAA and abrogated the activation of ERS. To determine whether IMD inhibited AAA by ameliorating ERS, we used 2 non-selective ERS inhibitors phenyl butyrate (4-PBA) and taurine (TAU). Similar to IMD, PBA, and TAU significantly reduced the incidence of AAA and AAA-related pathological disorders. In vitro, AngII infusion up-regulated CHOP, caspase12 expression and led to VSMC apoptosis. IMD siRNA aggravated the CHOP, caspase12-mediated VSMC apoptosis, which was abolished by ATF4 silencing. IMD infusion promoted the phosphorylation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) in aortas in ApoE KO mice, and the AMPK inhibitor compound C abolished the protective effect of IMD on VSMC ERS and apoptosis induced by AngII. In conclusion, IMD may protect against AAA formation by inhibiting ERS via activating AMPK phosphorylation.

Indexed as

Adenylate KinaseAngiotensin IIAnimalsAortic Aneurysm, AbdominalApolipoproteins EEndoplasmic Reticulum StressMiceMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MusclePeptide HormonesPhosphorylationAdenylate KinaseADM2 protein, humanAngiotensin IIApolipoproteins EPeptide HormonesAbdominal aortic aneurysmAMPKEndoplasmic reticulum stressIntermedinVSMC

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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.