Csengo Erika, Lorincz Hajnalka, Csosz Eva, Guba Andrea, Karai Bettina, Toth Judit, Csiha Sara, Paragh Gyorgy, Harangi Mariann, Nagy Gergely Gyorgy
Centre of Cardiovascular Diseases and Internal Medicine, Borsod-Abauj-Zemplen County Central Hospital and University Teaching Hospital, Szentpéteri kapu 72-76, 3526 Miskolc, Hungary.
Division of Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Int J Mol Sci. 2024 Dec 26;26(1):106. doi: 10.3390/ijms26010106.
Coenzyme Q10 (CoQ10) plays a crucial role in facilitating electron transport during oxidative phosphorylation, thus contributing to cellular energy production. Statin treatment causes a decrease in CoQ10 levels in muscle tissue as well as in serum, which may contribute to the musculoskeletal side effects. Therefore, we aimed to assess the effect of newly initiated statin treatment on serum CoQ10 levels after acute ST-elevation myocardial infarction (STEMI) and the correlation of CoQ10 levels with key biomarkers of subclinical or clinically overt myopathy. In this study, we enrolled 67 non-diabetic, statin-naïve early-onset STEMI patients with preserved renal function. Plasma CoQ10 level was determined by ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC/MS-MS), while the myopathy marker serum fatty acid-binding protein 3 (FABP3) level was measured with enzyme-linked immunosorbent assay (ELISA) at hospital admission and after 3 months of statin treatment. The treatment significantly decreased the plasma CoQ10 (by 43%) and FABP3 levels (by 79%) as well as total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B100 (ApoB100), and oxidized LDL (oxLDL) levels. The change in CoQ10 level showed significant positive correlations with the changes in total cholesterol, LDL-C, ApoB100, and oxLDL levels, while it did not correlate with the change in FABP3 level. Our results prove the CoQ10-reducing effect of statin treatment and demonstrate its lipid-lowering efficacy but contradict the role of CoQ10 reduction in statin-induced myopathy.
辅酶Q10（CoQ10）在氧化磷酸化过程中促进电子传递起着关键作用，从而有助于细胞能量的产生。他汀类药物治疗会导致肌肉组织和血清中CoQ10水平降低，这可能是肌肉骨骼副作用的原因之一。因此，我们旨在评估急性ST段抬高型心肌梗死（STEMI）后新开始的他汀类药物治疗对血清CoQ10水平的影响，以及CoQ10水平与亚临床或临床显性肌病关键生物标志物的相关性。在本研究中，我们纳入了67例肾功能正常的非糖尿病、未服用过他汀类药物的早发STEMI患者。采用超高效液相色谱-串联质谱法（UPLC/MS-MS）测定血浆CoQ10水平，同时在入院时和他汀类药物治疗3个月后，采用酶联免疫吸附测定法（ELISA）检测肌病标志物血清脂肪酸结合蛋白3（FABP3）水平。治疗显著降低了血浆CoQ10（降低43%）和FABP3水平（降低79%）以及总胆固醇、低密度脂蛋白胆固醇（LDL-C）、载脂蛋白B100（ApoB100）和氧化型LDL（oxLDL）水平。CoQ10水平的变化与总胆固醇、LDL-C、ApoB100和oxLDL水平的变化呈显著正相关，而与FABP3水平的变化无相关性。我们的结果证实了他汀类药物治疗降低CoQ10的作用，并证明了其降脂疗效，但与CoQ10降低在他汀类药物诱导的肌病中的作用相矛盾。
