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Can the NK Family of Osteoblast Homeodomain Transcription Factors Signaling Be a Magic Bullet to Reverse Calcification- Induced Vasculopathy in Diabetes?

机译:NK成骨细胞同源域转录因子信号传导家族能否成为逆转钙化诱导的糖尿病性血管病变的灵丹妙药?

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摘要

Human vascular calcification burden has existed for at least 5 millennia and has long been a major area of interest in the cardiovascular physiopathology research. Abnormal calcium deposition occurs in almost all arterial beds in both the media and intima in metabolic and diabetic diseases. Calcification of arteries reduces arterial elastance and compromises cardiovascular hemodynam-ics, which are high risk factors for cardiovascular diseases such stroke and ischemic heart disease. Despite the wealth of information regarding the effects of vascular calcification in atherosclerosis, metabolic syndrome, hypertension, and diabetes, the molecular mechanism of arteriosclerosis remains poorly understood. Therefore, understanding the mechanism by which diabetes and metabolic disease induce vascular calcification is crucial to identify effective new therapeutic strategies to intervene with the disease. Interestingly in this issue, Cheng et al.determined the in vivo contribution of members of the highly conserved NK family of osteoblast homeodomain transcription factors 1 (Msx1) and 2 (Msx2) signaling in arteriosclerosis and vascular stiffness in diabetic mice. The study by Cheng et al. provides new insight into the molecular mechanism that drives arteriosclerosis in diabetes and suggests a potential target for future therapy. Thus, targeting Msx1 and Msx2 would substantially help the development of a new therapeutic strategy to overcome calcification-induced vasculopathy.
机译:人体血管钙化负担已经存在至少5千年了,长期以来一直是心血管生理病理学研究的主要兴趣领域。在代谢性和糖尿病性疾病中,几乎所有中层和内膜的动脉床都会发生钙异常沉积。动脉钙化会降低动脉弹性并损害心血管血流动力学,这是心血管疾病(例如中风和缺血性心脏病)的高风险因素。尽管有大量关于血管钙化在动脉粥样硬化,代谢综合征,高血压和糖尿病中的作用的信息,但对动脉硬化的分子机制仍知之甚少。因此,了解糖尿病和代谢性疾病诱发血管钙化的机制对于确定干预该疾病的有效新治疗策略至关重要。有趣的是,Cheng等确定了糖尿病小鼠动脉硬化和血管僵硬中高度保守的NK成骨细胞同源域转录因子1(Msx1)和2(Msx2)信号传导成员的体内贡献。程等人的研究。提供了有关驱动糖尿病动脉硬化的分子机制的新见解,并提出了未来治疗的潜在目标。因此,靶向Msx1和Msx2将大大有助于开发一种新的治疗策略,以克服钙化引起的血管病。

著录项

  • 来源
    《Diabetes》 |2014年第12期|4011-4012|共2页
  • 作者单位

    Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA;

    Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-18 03:46:19

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