Mitochondrial-derived peptide MOTS-c attenuates vascular calcification and secondary myocardial remodeling via adenosine monophosphate-activated protein kinase signaling pathway
Open accessAbstract
INTRODUCTION: Vascular calcification (VC) is a complex, regulated process involved in many disease entities. So far, there are no treatments to reverse it. Exploring novel strategies to prevent VC is important and necessary for VC-related disease intervention. OBJECTIVE: In this study, we evaluated whether MOTS-c, a novel mitochondria-related 16-aa peptide, can reduce vitamin D3 and nicotine-induced VC in rats. METHODS: Vitamin D3 plus nicotine-treated rats were injected with MOTS-c at a dose of 5 mg/kg once a day for 4 weeks. Blood pressure, heart rate, and body weight were measured, and echocardiography was performed. The expression of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and the angiotensin II type 1 (AT-1) and endothelin B (ET-B) receptors was determined by Western blot analysis. RESULTS: Our results showed that MOTS-c treatment significantly attenuated VC. Furthermore, we found that the level of phosphorylated AMPK was increased and the expression levels of the AT-1 and ET-B receptors were decreased after MOTS-c treatment. CONCLUSIONS: Our findings provide evidence that MOTS-c may act as an inhibitor of VC by activating the AMPK signaling pathway and suppressing the expression of the AT-1 and ET-B receptors.
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Phosphorylated AMPK increased and the expression of endothelin B and angiotensin II receptor type 1 receptors decreased after MOTS-c treatment.
“In parallel, phosphorylated AMPK increased and the expression of endothelin B (ETB) and angiotensin II receptor type 1 (AT1) receptors decreased after MOTS-c treatment [136].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [136]
MOTS-c may act as an inhibitor of VCs via suppressing the expression of AT1 and ETB receptors, probably by activating AMPK signaling.
“These findings indicate that MOTS-c may act as an inhibitor of VCs via suppressing the expression of AT1 and ETB receptors, probably by activating AMPK signaling [136].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [136]
MOTS-c treatment significantly attenuated VCs induced by vitamin D3 and nicotine.
“Study showed that MOTS-c treatment significantly attenuated VCs induced by vitamin D3 and nicotine [136].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [136]
In a model of balloon-injured carotid arteries, TSPO expression was dramatically increased in carotid arteries.
“In a model of balloon-injured carotid arteries, TSPO expression was dramatically increased in carotid arteries [136].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [136]
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- Authors
- Wei, M., Gan, L., Liu, Z., Liu, L., Chang, J.-R., Yin, D.-C., Cao, H.-L., Su, X.-L., & Smith, W. W.
- Affiliations
- Xi'an Medical University (CN)
- Shaanxi Provincial People's Hospital (CN)
- Guilin Medical University (CN)
- Johns Hopkins University (US)
- Venue
- Cardiorenal Medicine
- Publisher
- S. Karger AG
- Published
- 2019-11-06
- Volume
- 10
- Issue
- 1
- Pages
- 42-50
- ISSN
- 1664-3828 (ISSN-L)
- 1664-5502
- OpenAlex
- W2997909611
- Cited by
- 52
- References
- 26
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 3 · 2023: 13 · 2022: 9 · 2021: 9 · 2020: 5
- FWCI
- 4.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cardiorenal Medicine (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81801414, 31400984)
- Natural Science Foundation of Guangxi Province (2018JJA140045)
- Fourth Military Medical University
- Xi'an Medical University
- Topics
- Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Keywords
- MOTS-c, mitochondrial peptides, vascular calcification, AMPK signaling, cardiac remodeling, angiotensin II type 1 receptor, endothelin B receptor, vitamin D3, nicotine, hypertension, echocardiography
- MeSH terms
- Animals, Cholecalciferol, Male, Nicotine, Signal Transduction, Rats, Sprague-Dawley, Ventricular Remodeling, Models, Animal, Mitochondrial Proteins, Receptor, Endothelin B, Receptor, Angiotensin, Type 1, Rats, AMP-Activated Protein Kinases, Vascular Calcification
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