Melatonin alleviates myocardial dysfunction through inhibition of endothelial-to-mesenchymal transition via the NF-κB pathwayopen access
- Authors
- Kim, Ran; Kim, Minsuk; Jeong, Seongtae; Kim, Sejin; Moon, Hanbyeol; Kim, Hojin; Lee, Min Young; Kim, Jongmin; Kim, Hyung-Sik; Choi, Murim; Shin, Kunyoo; Song, Byeong-Wook; Chang, Woochul
- Issue Date
- May-2024
- Publisher
- WILEY
- Keywords
- cardioprotection; endothelial dysfuction; endothelial to mesenchymal transition; melatonin; myocardial infarction; NF-kappa B pathway
- Citation
- JOURNAL OF PINEAL RESEARCH, v.76, no.4
- Journal Title
- JOURNAL OF PINEAL RESEARCH
- Volume
- 76
- Number
- 4
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/160161
- DOI
- 10.1111/jpi.12958
- ISSN
- 0742-3098
1600-079X
- Abstract
- Endothelial-to-mesenchymal transition (EndMT) is a complex biological process of cellular transdifferentiation by which endothelial cells (ECs) lose their characteristics and acquire mesenchymal properties, leading to cardiovascular remodeling and complications in the adult cardiovascular diseases environment. Melatonin is involved in numerous physiological and pathological processes, including aging, and has anti-inflammatory and antioxidant activities. This molecule is an effective therapeutic candidate for preventing oxidative stress, regulating endothelial function, and maintaining the EndMT balance to provide cardiovascular protection. Although recent studies have documented improved cardiac function by melatonin, the mechanism of action of melatonin on EndMT remains unclear. The present study investigated the effects of melatonin on induced EndMT by transforming growth factor-beta 2/interleukin-1 beta in both in vivo and in vitro models. The results revealed that melatonin reduced the migratory ability and reactive oxygen species levels of the cells and ameliorated mitochondrial dysfunction in vitro. Our findings indicate that melatonin prevents endothelial dysfunction and inhibits EndMT by activating related pathways, including nuclear factor kappa B and Smad. We also demonstrated that this molecule plays a crucial role in restoring cardiac function by regulating the EndMT process in the ischemic myocardial condition, both in vessel organoids and myocardial infarction (MI) animal models. In conclusion, melatonin is a promising agent that attenuates EC dysfunction and ameliorates cardiac damage compromising the EndMT process after MI.
- Files in This Item
-
Go to Link
- Appears in
Collections - 이과대학 > 생명시스템학부 > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/160161)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.