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Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regeneration via DUSP1 ADP-ribosylation-mediated p38 MAPK phosphorylation

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收录情况： ◇ SCIE ◇ 统计源期刊 ◇ CSCD-C ◇ 卓越：领军期刊

作者：
Tang Luxun[1,2,3] * ; Shi Yu[1,2] * ; Liao Qiao[1,2] * ; Wang Feng[1,2] ; Wu Hao[1,2] ; Ren Hongmei[1,2] ; Wang Xuemei[1,2] ; Fu Wenbin[1,2] ; Shou Jialing[1,2] ; Wang Wei Eric[1,2] ; Jose Pedro A[4] ; Yang Yongjian[3] ; Zeng Chunyu[1,2,5,6,7] ;
机构： [1]Department of Cardiology, Daping Hospital, the Third Military Medical University (Army Medical University), Chongqing 400042, China. [2]Key Laboratory of Geriatric Cardiovascular and Cerebrovascular Disease Research, Ministry of Education of China, Chongqing Key Laboratory for Hypertension Research, Chongqing Cardiovascular Clinical Research Center, Chongqing Institute of Cardiology, Chongqing 400042, China. [3]Department of Cardiovascular Medicine, the General Hospital of Western Theater Command, Chengdu 610083, China. [4]Division of Renal Diseases and Hypertension, the George Washington University School of Medicine and Health Sciences, Washington, DC 20541, USA. [5]State Key Laboratory of Trauma, Burns and Combined Injury, Daping Hospital, the Third Military Medical University, Chongqing 400042, China. [6]Cardiovascular Research Center of Chongqing College, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Chongqing 400042, China. [7]Department of Cardiology, the First Affiliated Hospital of Kunming Medical University, Kunming 650000, China.
出处：
DOI： 10.1016/j.apsb.2024.11.001
ISSN：

关键词： Metabolic reprogramming Cardiomyocyte proliferation Carnitine palmitoyltransferase 1 Etomoxir Fatty acid oxidation Glycolysis ADP-ribosylation p38 MAPK

摘要：
The neonatal mammalian heart has a remarkable regenerative capacity, while the adult heart has difficulty to regenerate. A metabolic reprogramming from glycolysis to fatty acid oxidation occurs along with the loss of cardiomyocyte proliferative capacity shortly after birth. In this study, we sought to determine if and how metabolic reprogramming regulates cardiomyocyte proliferation. Reversing metabolic reprogramming by carnitine palmitoyltransferase 1 (CPT1) inhibition, using cardiac-specific Cpt1a and Cpt1b knockout mice promoted cardiomyocyte proliferation and improved cardiac function post-myocardial infarction. The inhibition of CPT1 is of pharmacological significance because those protective effects were replicated by etomoxir, a CPT1 inhibitor. CPT1 inhibition, by decreasing poly(ADP-ribose) polymerase 1 expression, reduced ADP-ribosylation of dual-specificity phosphatase 1 in cardiomyocytes, leading to decreased p38 MAPK phosphorylation, and stimulation of cardiomyocyte proliferation. Our present study indicates that reversing metabolic reprogramming is an effective strategy to stimulate adult cardiomyocyte proliferation. CPT1 is a potential therapeutic target for promoting heart regeneration and myocardial infarction treatment.© 2025 The Authors.

基金：
This study was supported by grants from the National Key Research and Development Program of China (No. 2022YFA1104500), National Natural Science Foundation of China (No. 81930008), Natural Science Foundation of Sichuan Province (No. 2023NSFSC1651, China), and the National Institutes of Health (No. DK134574 and No. DK119652, US).
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外文
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出版当年[2026]版：
无
最新[2025]版：
大类 | 1 区 医学
小类 | 1 区 药学
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出版当年[2025]版：
无
最新[2024]版：
Q1 PHARMACOLOGY & PHARMACY

影响因子： 最新[2024版] 最新五年平均 出版当年[2025版] 出版当年五年平均 出版前一年[2024版]

第一作者：
第一作者机构： [1]Department of Cardiology, Daping Hospital, the Third Military Medical University (Army Medical University), Chongqing 400042, China. [2]Key Laboratory of Geriatric Cardiovascular and Cerebrovascular Disease Research, Ministry of Education of China, Chongqing Key Laboratory for Hypertension Research, Chongqing Cardiovascular Clinical Research Center, Chongqing Institute of Cardiology, Chongqing 400042, China. [3]Department of Cardiovascular Medicine, the General Hospital of Western Theater Command, Chengdu 610083, China.
共同第一作者：
通讯作者：
通讯机构： [1]Department of Cardiology, Daping Hospital, the Third Military Medical University (Army Medical University), Chongqing 400042, China. [2]Key Laboratory of Geriatric Cardiovascular and Cerebrovascular Disease Research, Ministry of Education of China, Chongqing Key Laboratory for Hypertension Research, Chongqing Cardiovascular Clinical Research Center, Chongqing Institute of Cardiology, Chongqing 400042, China. [5]State Key Laboratory of Trauma, Burns and Combined Injury, Daping Hospital, the Third Military Medical University, Chongqing 400042, China. [6]Cardiovascular Research Center of Chongqing College, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Chongqing 400042, China. [7]Department of Cardiology, the First Affiliated Hospital of Kunming Medical University, Kunming 650000, China.
推荐引用方式(GB/T 7714)：
Tang Luxun,Shi Yu,Liao Qiao,et al.Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regeneration via DUSP1 ADP-ribosylation-mediated p38 MAPK phosphorylation[J].Acta Pharmaceutica Sinica B.2025,15(1):256-277.doi:10.1016/j.apsb.2024.11.001.
APA：
Tang Luxun,Shi Yu,Liao Qiao,Wang Feng,Wu Hao...&Zeng Chunyu.(2025).Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regeneration via DUSP1 ADP-ribosylation-mediated p38 MAPK phosphorylation.Acta Pharmaceutica Sinica B,15,(1)
MLA：
Tang Luxun,et al."Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regeneration via DUSP1 ADP-ribosylation-mediated p38 MAPK phosphorylation".Acta Pharmaceutica Sinica B 15..1(2025):256-277

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