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

Ming Wei, Lu Gan, Zheng Liu, Li Liu, Jin Rui Chang, Da Chuan Yin, Hui Ling Cao, Xing Li Su, Wanli W. Smith

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)42-50
Number of pages9
JournalCardioRenal Medicine
Volume10
Issue number1
DOIs
StatePublished - Jan 1 2020

Keywords

  • Adenosine monophosphate-activated protein kinase
  • Angiotensin II type 1
  • Endothelin B
  • MOTS-c
  • Rat model of vascular calcification

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Urology

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