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Ca
Pub Date : 2019-12-31 DOI: 10.12987/9780300235258-002
Giusti, Palomeque, Mattiazzi
Diabetic cardiomyopathy is defined as the myocardial dysfunction that suffers patients with diabetes mellitus (DM) in the absence of hypertension and structural heart diseases such as valvular or coronary artery dysfunctions. Since the impact of DM on cardiac function is rather silent and slow, early stages of diabetic cardiomyopathy, known as prediabetes, are poorly recognized, and, on many occasions, cardiac illness is diagnosed only after a severe degree of dysfunction was reached. Therefore, exploration and recognition of the initial pathophysiological mechanisms that lead to cardiac dysfunction in diabetic cardiomyopathy are of vital importance for an on-time diagnosis and treatment of the malady. Among the complex and intricate mechanisms involved in diabetic cardiomyopathy, Ca2+ mishandling and mitochondrial dysfunction have been described as pivotal early processes. In the present review, we will focus on these two processes and the molecular pathway that relates these two alterations to the earlier stages and the development of diabetic cardiomyopathy.
糖尿病性心肌病被定义为糖尿病(DM)患者在没有高血压和心脏结构性疾病(如瓣膜或冠状动脉功能障碍)的情况下发生的心肌功能障碍。由于糖尿病对心功能的影响是相当沉默和缓慢的,因此早期的糖尿病心肌病,即前驱糖尿病,很少被认识到,并且在许多情况下,心脏病只有在达到严重的功能障碍程度后才被诊断出来。因此,探索和认识糖尿病性心肌病心功能障碍的初始病理生理机制,对及时诊断和治疗糖尿病性心肌病具有重要意义。在糖尿病心肌病的复杂和复杂的机制中,Ca2+处理不当和线粒体功能障碍被描述为关键的早期过程。在本文中,我们将重点关注这两个过程以及这两个改变与糖尿病性心肌病早期阶段和发展相关的分子途径。
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Frontmatter
Pub Date : 2019-12-31 DOI: 10.12987/9780300235258-fm
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We Play a Game
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