NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction.
NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction.
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DOI：
10.3390/antiox11091822
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发表时间：
2022-09-16
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--
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烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶调节活性氧（ROS）的产生，活性氧对细胞成分造成氧化损伤，但也调节许多细胞类型的氧化还原信号，在心血管系统中具有重要功能。过去几十年的研究已经揭示了NADPH氧化酶（NOX）在内皮细胞、平滑肌细胞、巨噬细胞、心肌细胞、成纤维细胞和其他细胞类型中调节氧化应激和细胞内信号传导的机制。例如，NOX2和NOX4调节心肌细胞中不同的氧化还原信号机制，与心脏肥厚和心力衰竭的发生和进展有关。保留射血分数的心力衰竭（HFpEF）至少占所有心力衰竭病例的一半，迄今为止几乎没有有效的治疗方法，通常与心室舒张功能障碍有关，即心室舒张和/或充盈缺陷。然而，HFpEF会影响多个器官系统，并与系统性病变相关，包括炎症、氧化应激、动脉硬化、心脏纤维化、肾脏、脂肪组织和骨骼肌功能障碍。基础科学研究和临床数据表明，全身和心肌氧化应激在HFpEF中起作用，动物模型的证据表明，NOX酶在舒张功能和几种HFpEF相关合并症中的关键作用。在这里，我们讨论了NOX酶在心血管细胞中的作用，它与舒张功能障碍和HFpEF的发生和进展有关，并概述了潜在的临床意义。
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases regulate production of reactive oxygen species (ROS) that cause oxidative damage to cellular components but also regulate redox signaling in many cell types with essential functions in the cardiovascular system. Research over the past couple of decades has uncovered mechanisms by which NADPH oxidase (NOX) enzymes regulate oxidative stress and compartmentalize intracellular signaling in endothelial cells, smooth muscle cells, macrophages, cardiomyocytes, fibroblasts, and other cell types. NOX2 and NOX4, for example, regulate distinct redox signaling mechanisms in cardiac myocytes pertinent to the onset and progression of cardiac hypertrophy and heart failure. Heart failure with preserved ejection fraction (HFpEF), which accounts for at least half of all heart failure cases and has few effective treatments to date, is classically associated with ventricular diastolic dysfunction, i.e., defects in ventricular relaxation and/or filling. However, HFpEF afflicts multiple organ systems and is associated with systemic pathologies including inflammation, oxidative stress, arterial stiffening, cardiac fibrosis, and renal, adipose tissue, and skeletal muscle dysfunction. Basic science studies and clinical data suggest a role for systemic and myocardial oxidative stress in HFpEF, and evidence from animal models demonstrates the critical functions of NOX enzymes in diastolic function and several HFpEF-associated comorbidities. Here, we discuss the roles of NOX enzymes in cardiovascular cells that are pertinent to the development and progression of diastolic dysfunction and HFpEF and outline potential clinical implications.
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