Toedebusch Ryan, Belenchia Anthony, Pulakat Lakshmi
Cardiovascular Medicine Division, Department of Medicine, University of Missouri, Columbia, MO, United States.
Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, United States.
Front Physiol. 2018 May 3;9:453. doi: 10.3389/fphys.2018.00453. eCollection 2018.
Diabetic cardiomyopathy refers to a unique set of heart-specific pathological variables induced by hyperglycemia and insulin resistance. Given that cardiovascular disease (CVD) is the leading cause of death in the world, and type 2 diabetes incidence continues to rise, understanding the complex interplay between these two morbidities and developing novel therapeutic strategies is vital. Two hallmark characteristics specific to diabetic cardiomyopathy are diastolic dysfunction and cardiac structural mal-adaptations, arising from cardiac cellular responses to the complex toxicity induced by hyperglycemia with or without hyperinsulinemia. While type 2 diabetes is more prevalent in men compared to women, cardiovascular risk is higher in diabetic women than in diabetic men, suggesting that diabetic women take a steeper path to cardiomyopathy and heart failure. Accumulating evidence from randomized clinical trials indicate that although pre-menopausal women have lower risk of CVDs, compared to age-matched men, this advantage is lost in diabetic pre-menopausal women, which suggests estrogen availability does not protect from increased cardiovascular risk. Notably, few human studies have assessed molecular and cellular mechanisms regarding similarities and differences in the progression of diabetic cardiomyopathy in men versus women. Additionally, most pre-clinical rodent studies fail to include female animals, leaving a void in available data to truly understand the impact of biological sex differences in diabetes-induced dysfunction of cardiovascular cells. Elegant reviews in the past have discussed in detail the roles of estrogen-mediated signaling in cardiovascular protection, sex differences associated with telomerase activity in the heart, and cardiac responses to exercise. In this review, we focus on the emerging cellular and molecular markers that define sex differences in diabetic cardiomyopathy based on the recent clinical and pre-clinical evidence. We also discuss miR-208a, MED13, and AT2R, which may provide new therapeutic targets with hopes to develop novel treatment paradigms to treat diabetic cardiomyopathy uniquely between men and women.
糖尿病性心肌病是指由高血糖和胰岛素抵抗引起的一组独特的心脏特异性病理变量。鉴于心血管疾病(CVD)是全球主要的死亡原因,且2型糖尿病的发病率持续上升,了解这两种疾病之间的复杂相互作用并开发新的治疗策略至关重要。糖尿病性心肌病的两个标志性特征是舒张功能障碍和心脏结构适应性不良,这是由心脏细胞对高血糖(无论有无高胰岛素血症)诱导的复杂毒性的反应所引起的。虽然2型糖尿病在男性中比女性更普遍,但糖尿病女性的心血管风险高于糖尿病男性,这表明糖尿病女性患心肌病和心力衰竭的风险更高。随机临床试验的越来越多的证据表明,尽管绝经前女性患心血管疾病的风险低于年龄匹配的男性,但糖尿病绝经前女性失去了这一优势,这表明雌激素的存在并不能预防心血管风险的增加。值得注意的是,很少有人类研究评估男性和女性糖尿病性心肌病进展中异同的分子和细胞机制。此外,大多数临床前啮齿动物研究未纳入雌性动物,从而在现有数据中留下空白,无法真正了解生物性别差异对糖尿病诱导的心血管细胞功能障碍的影响。过去已有详尽的综述讨论了雌激素介导的信号传导在心血管保护中的作用、与心脏端粒酶活性相关的性别差异以及心脏对运动的反应。在本综述中,我们基于最近的临床和临床前证据,重点关注定义糖尿病性心肌病性别差异的新出现的细胞和分子标志物。我们还讨论了miR-208a、MED13和AT2R,它们可能提供新的治疗靶点,有望开发新的治疗模式,以独特地治疗男性和女性的糖尿病性心肌病。