Versaci Francesco, Valenti Valentina, Forte Maurizio, Cammisotto Vittoria, Nocella Cristina, Bartimoccia Simona, Schirone Leonardo, Schiavon Sonia, Vecchio Daniele, D'Ambrosio Luca, Spinosa Giulia, D'Amico Alessandra, Chimenti Isotta, Violi Francesco, Frati Giacomo, Pignatelli Pasquale, Sciarretta Sebastiano, Pastori Daniele, Carnevale Roberto
Department of Cardiology, Santa Maria Goretti Hospital, 04100 Latina, Italy.
IRCCS Neuromed, 86077 Pozzilli, Italy.
Antioxidants (Basel). 2022 Apr 1;11(4):698. doi: 10.3390/antiox11040698.
Background: Aging is an independent risk factor for cardiovascular diseases. The autophagy process may play a role in delaying aging and improving cardiovascular function in aging. Data regarding autophagy in atrial fibrillation (AF) patients are lacking. Methods: A post hoc analysis of the prospective ATHERO-AF cohort study, including 150 AF patients and 150 sex- and age-matched control subjects (CS), was performed. For the analysis, the population was divided into three age groups: <50−60, 61−70, and >70 years. Oxidative stress (Nox2 activity and hydrogen peroxide, H2O2), platelet activation (PA) by sP-selectin and CD40L, endothelial dysfunction (nitric oxide, NO), and autophagy parameters (P62 and ATG5 levels) were assessed. Results: Nox2 activity and H2O2 production were higher in the AF patients than in the CS; conversely, antioxidant capacity was decreased in the AF patients compared to the CS, as was NO production. Moreover, sP-selectin and CD40L were higher in the AF patients than in the CS. The autophagy process was also significantly impaired in the AF patients. We found a significant difference in oxidative stress, PA, NO production, and autophagy across the age groups. Autophagy markers correlated with oxidative stress, PA, and endothelial dysfunction in both groups. Conclusions: This study provides evidence that the autophagy process may represent a mechanism for increased cardiovascular risk in the AF population.
衰老为心血管疾病的独立危险因素。自噬过程可能在延缓衰老及改善衰老过程中的心血管功能方面发挥作用。心房颤动（AF）患者自噬方面的数据尚缺。方法：对前瞻性ATHERO-AF队列研究进行事后分析，该研究纳入了150例AF患者及150例性别和年龄匹配的对照受试者（CS）。为进行分析，将人群分为三个年龄组：<50-60岁、61-70岁及>70岁。评估氧化应激（Nox2活性及过氧化氢，H2O2）、sP-选择素及CD40L介导的血小板活化（PA）、内皮功能障碍（一氧化氮，NO）及自噬参数（P62及ATG5水平）。结果：AF患者的Nox2活性及H2O2生成高于CS；相反，与CS相比，AF患者的抗氧化能力降低，NO生成亦降低。此外，AF患者的sP-选择素及CD40L高于CS。AF患者的自噬过程亦显著受损。我们发现各年龄组在氧化应激、PA、NO生成及自噬方面存在显著差异。两组中自噬标志物均与氧化应激、PA及内皮功能障碍相关。结论：本研究提供证据表明自噬过程可能是AF人群心血管风险增加的一种机制。
