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首页> 外文期刊>Cellular Signalling >Diabetes mellitus associated cardiovascular signalling alteration: A need for the revisit
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Diabetes mellitus associated cardiovascular signalling alteration: A need for the revisit

机译：糖尿病相关的心血管信号改变：需要重新审视

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Diabetes mellitus, a chronic metabolic disorder, is recognized as a root cause of cardiovascular disorders. A long-term and uncontrolled diabetes mellitus coincides with the cardiovascular signalling alteration, resulting in inadequacy of maintaining the cardiovascular physiology. Nitric oxide (NO) is an imperative mediator of cardiovascular physiology as its signalling is known to mediate vasodilatory, anti-platelet, anti-proliferative, and anti-inflammatory actions in vessels. In 1998, Robert Furchgott, Louis Ignarro and Ferid Murad received the Nobel Prize in Medicine or Physiology for their great discoveries concerning the role of NO (originally identified as endothelium-derived relaxing factor, EDRF) as a key signalling molecule in regulating cardiovascular physiology. The activation of phosphatidylinositol 3-kinase (PI3-K) further activates protein kinase B (PKB/Akt), which subsequently enhances eNOS activation and vascular NO generation. However, in recent studies a marked impairment in PI3-K/Akt-eNOS-NO signalling has been demonstrated in the condition of diabetes mellitus. Therefore, the defective PI3-K-Akt-eNOS-NO signalling pathways could make diabetic patients more vulnerable to cardiovascular disease pathology concerning the key functions of NO. Adenosine produced by cardiac cells has abilities to attenuate the proliferation of cardiac fibroblasts, inhibit collagen synthesis, and defend the myocardium against ischemia-reperfusion injury. However, diabetes mellitus is associated with enhanced unidirectional uptake of interstitial adenosine and reduced ability to release adenosine by cardiac cells during ATP deprivation. The reduced myocardial extracellular availability and increased uptake of adenosine could make diabetic subjects more susceptible to myocardial abnormalities. This review throws lights on diabetes mellitus-associated cardiovascular signalling alterations and their possible contribution to cardiovascular disease pathology.
机译：糖尿病是一种慢性代谢性疾病，被认为是心血管疾病的根本原因。长期不受控制的糖尿病与心血管信号改变相吻合，导致维持心血管生理机能不足。一氧化氮（NO）是心血管生理的重要介质，因为其信号介导血管舒张，抗血小板，抗增殖和抗炎作用。 1998年，Robert Furchgott，Louis Ignarro和Ferid Murad因其关于NO（最初被确定为内皮源性舒张因子，EDRF）作为调节心血管生理的关键信号分子的作用的重大发现而获得了诺贝尔医学或生理学奖。磷脂酰肌醇3-激酶（PI3-K）的激活进一步激活了蛋白激酶B（PKB / Akt），随后增强了eNOS激活和血管NO生成。然而，在最近的研究中，已经证明在糖尿病情况下PI3-K / Akt-eNOS-NO信号传导明显受损。因此，有缺陷的PI3-K-Akt-eNOS-NO信号通路可能使糖尿病患者更易患心血管疾病，涉及NO的关键功能。心脏细胞产生的腺苷具有减弱心脏成纤维细胞增殖，抑制胶原蛋白合成并保护心肌免受缺血-再灌注损伤的能力。然而，糖尿病与ATP剥夺过程中间质腺苷的单向摄取增强和心肌细胞释放腺苷的能力降低有关。心肌细胞外可用性的降低和腺苷摄取的增加可能使糖尿病患者更易患心肌异常。这篇综述揭示了糖尿病相关的心血管信号改变及其对心血管疾病病理的可能贡献。

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