Mitochondrial-Derived Peptide MOTS-c Attenuates Vascular Calcification and Secondary Myocardial Remodeling via Adenosine Monophosphate-Activated Protein Kinase Signaling Pathway | Zendy

Ming Wei | Zendy; Lu Gan | Zendy; Zheng Liu | Zendy; Li Liu | Zendy; Jin-Rui Chang | Zendy; DaChuan Yin | Zendy; Hui-Ling Cao | Zendy; Xing-li Su | Zendy; Wanli W. Smith | Zendy

Open Access

Mitochondrial-Derived Peptide MOTS-c Attenuates Vascular Calcification and Secondary Myocardial Remodeling via Adenosine Monophosphate-Activated Protein Kinase Signaling Pathway

Author(s) -

Ming Wei,

Lu Gan,

Zheng Liu,

Li Liu,

Jin-Rui Chang,

DaChuan Yin,

Hui-Ling Cao,

Xing-li Su,

Wanli W. Smith

Publication year - 2019

Publication title -

cardiorenal medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.661

H-Index - 21

eISSN - 1664-3828

pISSN - 1664-5502

DOI - 10.1159/000503224

Subject(s) - medicine , cyclic adenosine monophosphate , adenosine , protein kinase a , microbiology and biotechnology , adenosine monophosphate , signal transduction , cgmp dependent protein kinase , kinase , protein kinase c , biochemistry , chemistry , mitogen activated protein kinase kinase , biology , receptor

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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