动脉粥样硬化(AS)是心脑血管疾病的基础，高血压与糖尿病作为AS的危险因素促进其发生发展，泡沫细胞是AS的病理基础。镁及离子通道与AS密切相关，然而人们对高血压-糖尿病大鼠模型平滑肌源性泡沫细胞的镁(Mg2+)稳态和离子通道的调控缺乏认识。我们前期研究发现细胞内Mg2+影响Genistein对血管平滑肌细胞BKCa电流的作用。TRPM7作为调节Mg2+的重要通道，在平滑肌源性泡沫细胞中的机能状态和调控作用有待研究。因此，本课题应用膜片钳、分子生物学等实验技术，以高血压-糖尿病大鼠模型平滑肌源性泡沫细胞为研究对象，探索TRPM7通道酶的机能状态对镁稳态和BKCa通道的调控，及Genistein对TRPM7通道的调节和Mg2+对Genistein作用的影响，从崭新角度阐述平滑肌源性泡沫细胞中镁稳态和离子通道变化、相互调控及相关药物调节，为研究AS和缺血性脑血管病的发病机制和药物防治提供新思路。

Atherosclerosis (AS) plays a fundamental role in the pathogenesis of various cardiovascular and cerebrovascular diseases. Hypertension and diabetes as risk factors of AS contribute to its development, and foam cell formation is the pathological basis of AS. Also，magnesium and ion channels are closely related to AS. However, the modulation of magnesium (Mg2+) homeostasis and ion channel in smooth muscle cell-derived foam cells from hypertension-diabetes rat model is unknown. Our previous study found that intracellular Mg2+ influenced the effect of genistein (tyrosine kinase inhibitor) on BKCa current in vascular smooth muscle cells. TRPM7, as an important channel to moduate Mg2+, remains to be further studied about its functional status and regulatory role in smooth muscle cell-derived foam cells. By utilizting experimental techiniques such as patch clamp, molecular biology, cell culture, we use smooth muscle cell-derived foam cells from hypertension-diabetes rat model to explore the functional status of TRPM7 channel and its regulation of magnesium homeostasis and BKCa channels, and the effects of genistein on TRPM7 channel and how Mg2 + influences its effects. Our results will elucidate magnesium homeostasis and changes of ion channels, mutual regulation and drug adjustment in smooth muscle cell-derived foam cells from a new perspective and provide a novel viewpoint for the pathogenesis of AS and ischemic cerebrovascular disease as well as drug prevention.