Sarkar Subendu, Chopra Seema, Rohit Manoj Kumar, Banerjee Dibyajyoti, Chakraborti Anuradha
Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India.
Department of Obstetrics & Gynecology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India.
Med Hypotheses. 2016 Oct;95:62-66. doi: 10.1016/j.mehy.2016.09.001. Epub 2016 Sep 3.
Rheumatic heart disease (RHD) remains a major cause of cardiac related mortality and morbidity in the developing countries due to poor diagnosis and lack of proper therapeutics. The definite reason of heart valve injury during RHD is poorly understood. Valvular endothelial cells play an important role in pathogenesis of different cardiovascular diseases. Besides, the regulation of vitamin D (calciferol) and VEGF (vascular endothelial growth factor) results in the functional changes in endothelial cells. However, the crosstalk between vitamin D and VEGF in the pathogenesis of RHD is not yet unfurled. Evidences in the concerned fields are documented by searching through Google Scholar and Pubmed. Literature based survey has revealed that vascular endothelium, especially endothelial cells play important roles in valvular remodelling during cardiovascular diseases. Endothelial cell dysfunction leads to heart valve remodelling, which furthermore initiates the pathogenesis of valvular heart disease. Vitamin D has the potential to maintain the concentration of VEGF in the circulation and induce the function of endothelial cells. Hence, we hypothesize that vitamin D and VEGF homeostasis can alter the function of endothelial cells, which may subsequently trigger the valvular remodelling or even damage of heart valves during the progression of RHD pathogenesis. Our hypothesis shed light on the evidence based knowledge translation of plausible cellular phenomena due to vitamin D/VEGF homeostasis during valvular vandalism in RHD.
由于诊断不力和缺乏适当的治疗方法，风湿性心脏病（RHD）仍然是发展中国家心脏相关死亡率和发病率的主要原因。RHD期间心脏瓣膜损伤的确切原因尚不清楚。瓣膜内皮细胞在不同心血管疾病的发病机制中起重要作用。此外，维生素D（钙化醇）和血管内皮生长因子（VEGF）的调节会导致内皮细胞功能改变。然而，维生素D和VEGF在RHD发病机制中的相互作用尚未阐明。通过在谷歌学术和PubMed上搜索，记录了相关领域的证据。基于文献的调查表明，血管内皮，尤其是内皮细胞在心血管疾病期间的瓣膜重塑中起重要作用。内皮细胞功能障碍导致心脏瓣膜重塑，进而引发瓣膜性心脏病的发病机制。维生素D有可能维持循环中VEGF的浓度并诱导内皮细胞的功能。因此，我们假设维生素D和VEGF的稳态可以改变内皮细胞的功能，这可能随后在RHD发病机制进展过程中引发瓣膜重塑甚至心脏瓣膜损伤。我们的假设为RHD瓣膜破坏过程中由于维生素D/VEGF稳态导致的合理细胞现象的循证知识转化提供了线索。
