共查询到18条相似文献,搜索用时 78 毫秒
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自噬是真核细胞中普遍存在的一种物质降解途径,通过自噬溶酶体介导,清除自身多余或受损的细胞器,以维持细胞内物质的再循环并调节内环境稳态,对机体生长、发育和衰老均起重要作用。研究发现,自噬影响心血管功能,与心血管疾病的病理生理进程密切相关。本文从自噬的信号转导途径,自噬与糖尿病心肌的关系及其可能的机制的进行探讨,希望从自噬的角度对糖尿病心肌病的发生、发展过程进行阐述,为治疗糖尿病心肌病提供理论依据。 相似文献
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目的:观察鞘氨醇激酶1(Sphk1)在糖尿病性心肌病(DCM)大鼠中的自噬作用,为DCM的防治寻求新的靶点。方法:雄性Wistar大鼠20只被随机分为正常对照组(n=10)、DCM组(n=10)。腹腔注射链脲佐菌素(STZ)70mg/kg建立DCM大鼠模型。每2周观察大鼠体重、空腹血糖,8周后,检测两组左室舒张末期内径(LVEDd)、左室收缩末期内径(LVESd)、左室射血分数(LVEF)等;取心脏组织,行HE染色观察心脏形态。应用蛋白质印迹法检测Sphk1、自噬相关蛋白LC3II/LC3I、自噬相关蛋白Beclin 1表达水平。结果:造模8周后,与正常对照组比较,DCM组体重[(351±27)g比(198±11)g]显著降低,血糖[(6.84±0.93)mmol/L比(32.45±4.27)mmol/L]显著升高(P均=0.001);LVEDd[(7.12±0.36)mm比(6.46±0.28)mm]显著减小、LVESd[(3.39±0.14)mm比(3.72±0.25)mm]显著增加,LVEF值[(82.69±3.37)%比(62.50±3.08)%]显著降低(P<0.05或<0.01);Sphk1[(0.30±0.02)比(1.12±0.20)]、LC3II/LC3I[(0.44±0.05)比(1.03±0.14)]、Beclin 1[(0.35±0.08)比(0.73±0.12)]蛋白表达显著升高(P<0.05或<0.01)。HE染色可见心肌细胞增生肥大、排列紊乱。结论:Sphk1通过自噬促使大鼠的糖尿病性心肌病的发生发展。 相似文献
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糖尿病心肌病是糖尿病严重的心血管并发症之一,严重影响糖尿病患者的生活质量。其发病机制复杂,心肌代谢障碍、氧化应激和炎症反应等都与糖尿病患者的心脏功能障碍和心力衰竭的发展独立相关。近年来人们对糖尿病心肌病的研究和认识不断深入,现主要对糖尿病心肌病发病机制做一综述。 相似文献
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《中国老年学杂志》2017,(15)
目的探讨自噬在肾脏结石发病中的作用机制。方法建立腺嘌呤摄入过量引发的肾结石小鼠模型,通过对小鼠血液、尿液、肾脏组织样本收集,运用分子生物学方法检测小鼠血液中肌苷酸含量、小鼠体重、肾比重、一昼夜尿液量、小鼠尿液中微量蛋白含量及肾脏组织自噬基因mRNA和自噬相关蛋白的表达情况,并运用生物统计学进行数统计。结果腺嘌呤模型小鼠体重下降,肾比重和一昼夜排尿量比对照组较高,酶联免疫吸附(ELISA)结果显示腺嘌呤模型小鼠血液中肌苷酸的含量,尿液中微量蛋白的含量与对照组相比升高,同时PCR及蛋白免疫印迹结果证明自噬相关mRNA和蛋白表达量的变化,自噬抑制剂处理小鼠后,肾结石症状稍有缓解,自噬相关mRNA和蛋白表达量的也发生调整。结论证明2,8二羟基腺嘌呤结石的积累可以引起肾组织自噬发生,导致肾结石相关症状。 相似文献
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心肌致密化不全(Noncompaction cardiomyopathy,NCCM)是一种以是以心室内异常粗大的肌小梁和交错的深隐窝为特征的心肌病,患者在临床上以心力衰竭、恶性心律失常和血栓形成为主要表现,严重者可发生猝死。目前的治疗方法只能缓解症状,不能根治疾病。现有研究表明,基因突变是导致NCCM发生的重要原因,基因突变导致其编码的蛋白表达出现异常,干扰了心脏的正常发育。此外,NOTCH通路、TBX20/PRDM16/TGF-β通路等信号通路的异常参与了NCCM的发生发展。近年来,随着对基因表达调控研究的不断深入,表观遗传学已成为NCCM机制研究的新方向。本文旨在对NCCM的发病机制进行综述,以深刻理解NCCM发生发展的病理生理过程,为研究提供更多的思路。 相似文献
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Hiromitsu Kanamori Genki Naruse Akihiro Yoshida Shingo Minatoguchi Takatomo Watanabe Tomonori Kawaguchi Toshiki Tanaka Yoshihisa Yamada Hironobu Takasugi Atsushi Mikami Shinya Minatoguchi Tatsuhiko Miyazaki Hiroyuki Okura 《Journal of cardiology》2021,77(1):30-40
Diabetic cardiomyopathy, clinically diagnosed as ventricular dysfunction in the absence of coronary atherosclerosis or hypertension in diabetic patients, is a cardiac muscle-specific disease that increases the risk of heart failure and mortality. Its clinical course is characterized initially by diastolic dysfunction, later by systolic dysfunction, and eventually by clinical heart failure from an uncertain mechanism. Light microscopic features such as interstitial fibrosis, inflammation, and cardiomyocyte hypertrophy are observed in diabetic cardiomyopathy, but are common to failing hearts generally and are not specific to diabetic cardiomyopathy. Electron microscopic studies of biopsy samples from diabetic patients with heart failure have revealed that the essential mechanism underlying diabetic cardiomyopathy involves thickening of the capillary basement membrane, accumulation of lipid droplets, and glycogen as well as increased numbers of autophagic vacuoles within cardiomyocytes. Autophagy is a conserved mechanism that contributes to maintaining intracellular homeostasis by degrading long-lived proteins and damaged organelles and is observed more often in cardiomyocytes within failing hearts. Diabetes mellitus (DM) impairs cardiac metabolism and leads to dysregulation of energy substrates that contribute to cardiac autophagy. However, a “snapshot” showing greater numbers of autophagic vacuoles within cardiomyocytes may indicate that autophagy is activated into phagophore formation or is suppressed due to impairment of the lysosomal degradation step. Recent in vivo studies have shed light on the underlying molecular mechanism governing autophagy and its essential meaning in the diabetic heart. Autophagic responses to diabetic cardiomyopathy differ between diabetic types: they are enhanced in type 1 DM, but are suppressed in type 2 DM. This difference provides important insight into the pathophysiology of diabetic cardiomyopathy. Here, we review recent advances in our understanding of the pathophysiology of diabetic cardiomyopathy, paying particular attention to autophagy in the heart, and discuss the therapeutic potential of interventions modulating autophagy in diabetic cardiomyopathy. 相似文献
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糖尿病的发病率和患病率在全世界范围不断上升。糖尿病心肌病(DCM)是糖尿病主要的心脏并发症之一,其特征为左室舒张和(或)收缩功能障碍,也可伴有心力衰竭、心律失常、心源性休克,重症患者甚至猝死。DCM的发病机制尚未完全明确,目前认为其与心肌细胞的糖代谢、脂代谢与能量代谢异常,以及心肌纤维化、氧化应激和细胞死亡等多种因素有关。本文将从细胞、组织、分子水平等方面对DCM的发病机制的研究现状做一综述,以为临床防治提供依据。 相似文献
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糖尿病心肌病是排除了高血压、冠心病及其他已知疾病所致的心肌损伤而独立存在的病理生理状态,表现为心脏收缩和(或)舒张功能障碍。其发病机制还不清楚,目前发现与心肌细胞代谢障碍和结构异常、支配心肌的微小血管和自主神经功能紊乱等有关。目前还没有一种特异的诊断方法,一些新的技术包括多普勒组织成像技术、定量组织速度显像和心肌背向散射积分等逐渐应用于临床。本文旨在阐述糖尿病心肌病发病机制和诊断方法的新进展。 相似文献
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心血管疾病是2型糖尿病的主要并发症,约占2型糖尿病患者死亡人数的2/3。血糖异常、血脂异常、胰岛素抵抗、慢性低度炎症、氧化应激、内皮功能障碍、血管钙化和高凝状态等多种病理生理过程可加快2型糖尿病患者糖尿病心脏病的进展。糖尿病性心肌病是糖尿病心脏病中较为常见的一种,可导致心功能异常并最终进展为心力衰竭、心律失常,甚至猝死。本文综述了糖尿病性心肌病的发病机制,以及当前及未来潜在的治疗方法。 相似文献
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Research on the pathogenesis of nonischemic dilated cardiomyopathy (DCM) has largely been focused on the role of viral pathogens and altered immunity. Trace elements have only rarely been considered; however, clinical observations that trace elements influence cardiovascular disease have been made in populations with extreme dietary deficiency or occupational exposure. Recently, animal models of DCM have been used to explore interactions among trace elements, viral pathogens, and the immune system. Discovery of interactions of trace elements with causes for DCM has heightened awareness of potential contributions of environmental variables to DCM pathogenesis. This article reviews the present knowledge regarding trace elements, in particular selenium and mercury, in the pathogenesis of viral and immune-mediated DCM. Based on recent studies, the authors propose a novel paradigm for the pathogenesis of viral DCM that incorporates trace element imbalance and its interactions with the cellular physiology of viral-induced cardiomyocyte dysfunction. 相似文献