Muñoz-Córdova Felipe, Hernández-Fuentes Carolina, Lopez-Crisosto Camila, Troncoso Mayarling F, Calle Ximena, Guerrero-Moncayo Alejandra, Gabrielli Luigi, Chiong Mario, Castro Pablo F, Lavandero Sergio
Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, Advanced Center for Chronic Diseases (ACCDiS), University of Chile, Santiago, Chile.
Division of Cardiovascular Diseases, Faculty of Medicine, Advanced Center for Chronic Diseases (ACCDiS), Pontifical Catholic University of Chile, Santiago, Chile.
Front Cardiovasc Med. 2021 Dec 23;8:707336. doi: 10.3389/fcvm.2021.707336. eCollection 2021.
Diabetic cardiomyopathy (DCM) is a severe complication of diabetes developed mainly in poorly controlled patients. In DCM, several clinical manifestations as well as cellular and molecular mechanisms contribute to its phenotype. The production of reactive oxygen species (ROS), chronic low-grade inflammation, mitochondrial dysfunction, autophagic flux inhibition, altered metabolism, dysfunctional insulin signaling, cardiomyocyte hypertrophy, cardiac fibrosis, and increased myocardial cell death are described as the cardinal features involved in the genesis and development of DCM. However, many of these features can be associated with broader cellular processes such as inflammatory signaling, mitochondrial alterations, and autophagic flux inhibition. In this review, these mechanisms are critically discussed, highlighting the latest evidence and their contribution to the pathogenesis of DCM and their potential as pharmacological targets.
糖尿病性心肌病（DCM）是糖尿病的一种严重并发症，主要发生在血糖控制不佳的患者中。在DCM中，多种临床表现以及细胞和分子机制共同促成了其表型。活性氧（ROS）的产生、慢性低度炎症、线粒体功能障碍、自噬流抑制、代谢改变、胰岛素信号功能失调、心肌细胞肥大、心脏纤维化以及心肌细胞死亡增加，被描述为参与DCM发生和发展的主要特征。然而，这些特征中的许多都可能与更广泛的细胞过程相关，如炎症信号传导、线粒体改变和自噬流抑制。在本综述中，将对这些机制进行批判性讨论，突出最新证据及其对DCM发病机制的贡献以及它们作为药理学靶点的潜力。
