정성태 (가톨릭관동대학교) | 한빛사논문 > 한빛사

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정성태Seongtae Jeong

가톨릭관동대학교

J. Pineal Res., May 2024, 76 (4) | https://doi.org/10.1111/jpi.12958 Melatonin alleviates myocardial dysfunction through inhibition of endothelial-to-mesenchymal transition via the NF-κB pathway

Ran Kim¹, Minsuk Kim¹, Seongtae Jeong², Sejin Kim¹, Hanbyeol Moon², Hojin Kim², Min Young Lee³, Jongmin Kim⁴, Hyung‐Sik Kim⁵, Murim Choi⁶, Kunyoo Shin⁷, Byeong‐Wook Song², Woochul Chang¹

¹Department of Biology Education, College of Education, Pusan National University, Busan, South Korea

²Institute for Bio‐Medical Convergence, Catholic Kwandong University International St. Mary's Hospital, Incheon, South Korea

³Department of Molecular Physiology, College of Pharmacy, Kyungpook National University, Daegu, South Korea

⁴Department of Life Systems, Sookmyung Women's University, Seoul, Korea

⁵Department of Oral Biochemistry, Dental and Life Science Institute, School of Dentistry, Pusan National University, Yangsan, South Korea

⁶Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea

⁷School of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, South Korea

Ran Kim, Minsuk Kim, and Seongtae Jeong contributed to this work.

Correspondence : Woochul Chang, Byeong‐Wook Song

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-β2/interleukin-1β 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.

논문정보

형식Research article
게재일2024년 05월 (BRIC 등록일 2024-05-16)
연구진국내 연구진
분야 생명과학 > 생리학

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