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Angiotensin II affects inflammation mechanisms via AMPK-related signalling pathways in HL-1 atrial myocytes
Open accessAbstract
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.
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ETB and AT1 are involved in AMPK pathway by binding to their receptors.
“ETB and AT1 are reportedly involved in AMPK pathway by binding to their receptors [194,195].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [194]
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References 54 · Cited by 39
Metadata
- Authors
- Kim, N., Jung, Y., Nam, M., Sun Kang, M., Lee, M. K., Cho, Y., Choi, E.-K., Hwang, G.-S., & Soo Kim, H.
- Affiliations
- Korea Basic Science Institute (KR)
- Seoul National University (KR)
- Ewha Womans University (KR)
- Corresponding author
- Hwang, Geum-Sook
- Venue
- Scientific Reports
- Published
- 2017-09-04
- Volume
- 7
- Issue
- 1
- Pages
- 10328-10328
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5583339
- OpenAlex
- W2751387597
- Cited by
- 39
- References
- 54
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 8 · 2023: 5 · 2022: 1 · 2021: 8 · 2020: 3 · 2019: 5 · 2018: 4
- FWCI
- 2.54
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Research Foundation
- Korea University
- Korea Basic Science Institute (CAP-12-2-KBSI, C37705)
- National Research Foundation of Korea (2013M3A9B6046418, NRF-2016R1A2B4014418)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- angiotensin II, cardiac inflammation, AMPK signaling, JNK phosphorylation, TGF-β1, TNF-α, reactive oxygen species, oxidative stress, intracellular calcium, angiotensin II type 1 receptor, atrial myocytes, atrial fibrillation, oxygen consumption
- MeSH terms
- Angiotensin II, Calcium, Cell Survival, Heart Atria, Humans, Mitochondria, Myocarditis, Oxygen, Oxygen Consumption, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Myocytes, Cardiac, Receptor, Angiotensin, Type 1, AMP-Activated Protein Kinases
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