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亚精胺增强线粒体功能并减轻主动脉瓣钙化：对DNA甲基转移酶-1活性的影响。

Spermidine Enhances Mitochondrial Function and Mitigates Aortic Valve Calcification: Implications for DNA Methyltransferase-1 Activity.

作者信息

Song Naaleum, Ji Eunhye, Yu Jeong Eun, Choi Kyoung-Hee, Kim Dae-Hee, Song Jong-Min, Kang Duk-Hyun, Song Jae-Kwan, Yu Jiyoung, Kim Kyunggon, Lee Sahmin, Aikawa Elena

机构信息

Division of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; Department of Medical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Division of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.

出版信息

JACC Basic Transl Sci. 2025 Mar;10(3):345-366. doi: 10.1016/j.jacbts.2024.11.011. Epub 2025 Feb 12.

DOI:10.1016/j.jacbts.2024.11.011
PMID:40139876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12013848/
Abstract

Aortic stenosis (AS) is a severe heart valve disease marked by calcification, leading to heart failure. This study examined mitochondrial function in human aortic valve interstitial cells isolated from patients with AS and tested spermidine, an autophagy inducer as AS treatment. Spermidine treatment reduced fibrosis and calcification in human aortic valve interstitial cells and improved these features in spermidine-treated mice. The AKT-TP53-DNMT1-PPARG pathway was implicated, and DNA methyltransferase 1 inhibition by 5-azacytidine enhanced mitochondrial biogenesis by reducing mitochondrial DNA hypermethylation. These findings suggest that spermidine or DNA methyltransferase 1 inhibition could prevent aortic valve disease by improving mitochondrial function.

摘要

主动脉瓣狭窄（AS）是一种以钙化为主的严重心脏瓣膜疾病，可导致心力衰竭。本研究检测了从AS患者中分离出的人主动脉瓣间质细胞的线粒体功能，并测试了作为AS治疗药物的自噬诱导剂亚精胺。亚精胺治疗可减少人主动脉瓣间质细胞中的纤维化和钙化，并改善亚精胺治疗小鼠的这些特征。研究涉及AKT-TP53-DNMT1-PPARG通路，5-氮杂胞苷对DNA甲基转移酶1的抑制通过减少线粒体DNA高甲基化增强了线粒体生物合成。这些发现表明，亚精胺或DNA甲基转移酶1抑制可通过改善线粒体功能预防主动脉瓣疾病。

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