Evidence map›Paper›PMID 31186446›Full record

ArticleScientific reports2019

Angiotensin II Increases Endoplasmic Reticulum Stress in Adipose Tissue and Adipocytes.

Kalhara R Menikdiwela, Latha Ramalingam, London Allen, Shane Scoggin, Nishan S Kalupahana, Naima Moustaid-Moussa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Adipocyte · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
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  17. Review
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  19. Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  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

6 authors at 2 institutions in 2 countries.

Kalhara R MenikdiwelaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA.
Latha RamalingamDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA.
London AllenDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA.
Shane ScogginDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA.
Nishan S KalupahanaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA.ORCID http://orcid.org/0000-0001-7129-5588
Naima Moustaid-MoussaDepartment of Nutritional Sciences, Texas Tech University, Lubbock, Texas, USA. naima.moustaid-moussa@ttu.edu.ORCID http://orcid.org/0000-0002-7508-8030
Texas Tech University · USUniversity of Peradeniya · LK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Renin Angiotensin System (RAS), a key regulator of blood pressure has been linked to metabolic disorders. We have previously reported that adipose overexpression of angiotensinogen in mice (Agt-Tg) induces obesity, in part mediated by adipose tissue inflammation, through yet unidentified mechanisms. Hence, we hypothesize that adipose tissue enrichment of angiotensinogen leads to activation of inflammatory cascades and endoplasmic reticulum (ER) stress, thereby, contributing to obesity. We used wild type (Wt), Agt-Tg and Agt-knockout (KO) mice along with 3T3-L1 and human adipocytes treated with RAS, ER stress and inflammation inhibitors. ER stress and pro-inflammation markers were significantly higher in Agt-Tg compared to Wt mice and captopril significantly reduced their expression. Furthermore, in vitro treatment with Ang II significantly induced ER stress and inflammation, whereas angiotensin II receptor inhibitor, telmisartan reduced RAS effects. Moreover, miR-30 family had significantly lower expression in Agt-Tg group. MiR-708-5p and -143-3p were upregulated when RAS was overexpressed, and RAS antagonists reduced miR-143-3p and -708-5p in both mouse adipose tissue and adipocytes. Activation of RAS by Ang II treatment, increased inflammation and ER stress in adipocytes mainly via AT1 receptor, possibly mediated by miR-30 family, -708-5p and/or -143-3p. Hence, RAS and mediating microRNAs could be used as potential targets to reduce RAS induced obesity and related comorbid diseases.

Indexed as

3T3-L1 CellsAdipocytesAdipose TissueAngiotensin IIAnimalsCaptoprilDietEndoplasmic Reticulum StressHumansInflammationMiceMice, TransgenicMicroRNAsNF-kappa BRenin-Angiotensin SystemYY1 Transcription FactorAngiotensin IICaptoprilMicroRNAsNF-kappa BYY1 Transcription Factor

Identifiers

PMID31186446
PMCPMC6560092
OpenAlexW2951580636

What OpenQuestion holds

Textmetadata
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.