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左旋肉碱通过改善心肌细胞脂质沉积减轻高尿酸血症相关的左心室重构。

L-carnitine attenuated hyperuricemia-associated left ventricular remodeling through ameliorating cardiomyocytic lipid deposition.

作者信息

Yang Yang, Lin Cuiting, Zheng Qiang, Zhang Leqi, Li Yongmei, Huang Qinghua, Wu Ting, Zhao Zean, Li Lu, Luo Jian, Jiang Yanqing, Zhang Qun, Wang Xing, Xia Chenglai, Pang Jianxin

机构信息

Affiliated Foshan Maternity & Child Healthcare Hospital, Southern Medical University, Foshan, Guangdong, China.

School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, China.

出版信息

Front Pharmacol. 2023 Jan 31;14:1016633. doi: 10.3389/fphar.2023.1016633. eCollection 2023.

DOI:10.3389/fphar.2023.1016633
PMID:36817129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9929955/
Abstract

Hyperuricemia (HUA) is associated with left ventricular remodeling (LVR) and thereby causes the initiation and development of a large number of cardiovascular diseases. LVR is typically accompanied by cardiomyocyte energy metabolic disorder. The energy supply of cardiomyocytes is provided by glucose and fatty acid (FA) metabolism. Currently, the effect of HUA on cardiomyocytic FA metabolism is unclear. In this study, we demonstrate that UA-induced cardiomyocyte injury is associated with cytoplasmic lipid deposition, which can be ameliorated by the FA metabolism-promoting drug L-carnitine (LC). UA suppresses carnitine palmitoyl transferase 1B (CPT1B), thereby inhibiting FA transport into the mitochondrial inner matrix for elimination. LC intervention can ameliorate HUA-associated left ventricular anterior wall thickening in mice. This study showed that FA transport dysfunction plays is a critical mechanism in both cardiomyocytic injury and HUA-associated LVR and promoting cytoplasmic FA transportation through pharmacological treatment by LC is a valid strategy to attenuate HUA-associated LVR.

摘要

高尿酸血症（HUA）与左心室重构（LVR）相关，从而引发大量心血管疾病的发生和发展。LVR通常伴有心肌细胞能量代谢紊乱。心肌细胞的能量供应由葡萄糖和脂肪酸（FA）代谢提供。目前，HUA对心肌细胞FA代谢的影响尚不清楚。在本研究中，我们证明尿酸（UA）诱导的心肌细胞损伤与细胞质脂质沉积有关，而促进FA代谢的药物L-肉碱（LC）可改善这种情况。UA抑制肉碱棕榈酰转移酶1B（CPT1B），从而抑制FA转运至线粒体内基质进行清除。LC干预可改善小鼠HUA相关的左心室前壁增厚。本研究表明，FA转运功能障碍在心肌细胞损伤和HUA相关的LVR中均起关键作用，通过LC药物治疗促进细胞质FA转运是减轻HUA相关LVR的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/42f6b6726d08/fphar-14-1016633-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/6ac950112f0b/fphar-14-1016633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/c1772333aee9/fphar-14-1016633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/ce8809f48569/fphar-14-1016633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/5632904bb3fd/fphar-14-1016633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/19d2b1f34c9f/fphar-14-1016633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/42f6b6726d08/fphar-14-1016633-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/6ac950112f0b/fphar-14-1016633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/c1772333aee9/fphar-14-1016633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/ce8809f48569/fphar-14-1016633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/5632904bb3fd/fphar-14-1016633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/19d2b1f34c9f/fphar-14-1016633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5276/9929955/42f6b6726d08/fphar-14-1016633-g006.jpg

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