Evidence map›Paper›PMID 28871102›Full record

ArticleScientific reports2017

Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes.

Nami Kim, Youngae Jung, Miso Nam, Mi Sun Kang, Min Kyung Lee, Youngjin Cho, Eue-Keun Choi, Geum-Sook Hwang, Hyeon Soo Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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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 5 institutions in 1 country.

Nami KimIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea.
Youngae JungIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea.
Miso NamIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea.
Mi Sun KangIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea.
Min Kyung LeeIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea.
Youngjin ChoDivision of Cardiology, Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
Eue-Keun ChoiDivision of Cardiology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea.
Geum-Sook HwangIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, 120-140, Republic of Korea. gshwang@kbsi.re.kr.
Hyeon Soo KimDepartment of Anatomy, Korea University College of Medicine, Seoul, 02841, Republic of Korea. anatomykim@korea.ac.kr.
Korea Basic Science Institute · KREwha Womans University · KRKorea University · KRSeoul National University Bundang Hospital · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a common cause of cardiac arrhythmia. Angiotensin ІІ (Ang ІІ) is a major contributing factor in the pathogenesis of cardiac inflammation; however, its underlying molecular mechanism remains unclear. Here, we explored the effect of Ang ІІ on inflammatory mechanisms and oxidative stress using HL-1 atrial myocytes. We showed that Ang ІІ activated c-Jun N-terminal kinase (JNK) phosphorylation and other inflammatory markers, such as transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α). Ang ІІ decreased oxygen consumption rate, which resulted in reactive oxygen species (ROS) generation and inhibition of ROS blocked Ang II-mediated JNK phosphorylation and TGF-β1 induction. Ang ІІ induced the expression of its specific receptor, AT1R. Ang II-induced intracellular calcium production associated with Ang ІІ-mediated signalling pathways. In addition, the generated ROS and calcium stimulated AMPK phosphorylation. Inhibiting AMPK blocked Ang II-mediated JNK and TGF-β signalling pathways. Ang ІІ concentration, along with TGF-β1 and tumor necrosis factor-α levels, was slightly increased in plasma of patients with atrial fibrillation. Taken together, these results suggest that Ang ІІ induces inflammation mechanisms through an AMPK-related signalling pathway. Our results provide new molecular targets for the development of therapeutics for inflammation-related conditions, such as atrial fibrillation.

Indexed as

Signal TransductionAMP-Activated Protein KinasesAngiotensin IICalciumCell SurvivalHeart AtriaHumansMitochondriaMyocarditisMyocytes, CardiacOxidative StressOxygenOxygen ConsumptionReactive Oxygen SpeciesReceptor, Angiotensin, Type 1AMP-Activated Protein KinasesAngiotensin IICalciumOxygenReactive Oxygen SpeciesReceptor, Angiotensin, Type 1

Identifiers

PMID28871102
PMCPMC5583339
OpenAlexW2751387597

What OpenQuestion holds

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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.