论文库首页  论文库
 
论文编号:
论文题目: Myocardial infarction accelerates glomerular injury and microalbuminuria in diabetic rats via local hemodynamics and immunity
英文论文题目: Myocardial infarction accelerates glomerular injury and microalbuminuria in diabetic rats via local hemodynamics and immunity
第一作者: Dong, ZF; Gong, KZ; Huang, D; Zhu, W; Sun, WF; Zhang, Y; Xin, P; Shen, Y; Wu, PL; Li, JB; Lu, ZG; Zhang, XM; Wei, M
英文第一作者: Dong, ZF; Gong, KZ; Huang, D; Zhu, W; Sun, WF; Zhang, Y; Xin, P; Shen, Y; Wu, PL; Li, JB; Lu, ZG; Zhang, XM; Wei, M
联系作者: Wei, M (reprint author), Shanghai Jiao Tong Univ, Shanghai Hosp 6, Sch Med, Div Cardiol, 600 St Yishan, Shanghai 200233, Peoples R China.
英文联系作者: Wei, M (reprint author), Shanghai Jiao Tong Univ, Shanghai Hosp 6, Sch Med, Div Cardiol, 600 St Yishan, Shanghai 200233, Peoples R China.
外单位作者单位:
英文外单位作者单位:
发表年度: 2015
卷: 179
期:
页码: 397-408
摘要: Background: Clinically, approximately one-third of patients with chronic heart failure (CHF) exhibit some degree of renal dysfunction. This renal dysfunction is referred to as cardiorenal syndrome (CRS) and plays an important role in the poor prognosis of CHF. Mounting evidence suggests that diabetes is the most common underlying risk factor for CRS. However, the underlying pathophysiological mechanisms are poorly understood. Methods: We performed the following comparisons in two separate protocols: 1) surgically induced myocardial infarction rats (MI, n = 10), sham operation rats (Ctr, n = 10) and MI rats treated with Fasudil, a Rho-kinase inhibitor (MI + Fas, n = 9); and 2) STZ-induced type 1 diabetic rats (DB, n = 10), DB + MI rats (n = 10) and DB+ MI rats treated with Fasudil (DB + MI+ Fas, n = 9). Renal hemodynamics and vasoconstrictor reactivity were evaluated using the DMT myograph system. Renal immunity was evaluated by flow cytometry, electron microscopy, immunofluorescence, etc. Results: Twelve weeks after the operation, compared with DB or MI rats, DB + MI rats exhibited the following characteristics: 1) significantly increased glomerular enlargement, fibrosis, glomerulosclerosis, podocyte injury and microalbuminuria; 2) significantly increased vasoconstrictor reactivity of the renal interlobular arteries and renal venous pressure; 3) significantly increased infiltration of CD3+ and CD4+ T cells and decreased Treg/Th17 ratios; and 4) significantly increased glomerular deposition of IgG and C-4. In contrast, rats with MI only showed mildly accelerated glomerular remodeling and microalbuminuria, with little change in renal hemodynamics and immunity. Fasudil treatment significantly improved the renal lesions in DB+ MI rats but not MI rats. Conclusions: Post-MI cardiac dysfunction significantly accelerated glomerular remodeling, podocyte injury and microalbuminuria in STZ-induced diabetic rats. These changes were accompanied by altered local hemodynamics and immunity. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
英文摘要: Background: Clinically, approximately one-third of patients with chronic heart failure (CHF) exhibit some degree of renal dysfunction. This renal dysfunction is referred to as cardiorenal syndrome (CRS) and plays an important role in the poor prognosis of CHF. Mounting evidence suggests that diabetes is the most common underlying risk factor for CRS. However, the underlying pathophysiological mechanisms are poorly understood. Methods: We performed the following comparisons in two separate protocols: 1) surgically induced myocardial infarction rats (MI, n = 10), sham operation rats (Ctr, n = 10) and MI rats treated with Fasudil, a Rho-kinase inhibitor (MI + Fas, n = 9); and 2) STZ-induced type 1 diabetic rats (DB, n = 10), DB + MI rats (n = 10) and DB+ MI rats treated with Fasudil (DB + MI+ Fas, n = 9). Renal hemodynamics and vasoconstrictor reactivity were evaluated using the DMT myograph system. Renal immunity was evaluated by flow cytometry, electron microscopy, immunofluorescence, etc. Results: Twelve weeks after the operation, compared with DB or MI rats, DB + MI rats exhibited the following characteristics: 1) significantly increased glomerular enlargement, fibrosis, glomerulosclerosis, podocyte injury and microalbuminuria; 2) significantly increased vasoconstrictor reactivity of the renal interlobular arteries and renal venous pressure; 3) significantly increased infiltration of CD3+ and CD4+ T cells and decreased Treg/Th17 ratios; and 4) significantly increased glomerular deposition of IgG and C-4. In contrast, rats with MI only showed mildly accelerated glomerular remodeling and microalbuminuria, with little change in renal hemodynamics and immunity. Fasudil treatment significantly improved the renal lesions in DB+ MI rats but not MI rats. Conclusions: Post-MI cardiac dysfunction significantly accelerated glomerular remodeling, podocyte injury and microalbuminuria in STZ-induced diabetic rats. These changes were accompanied by altered local hemodynamics and immunity. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
刊物名称: INTERNATIONAL JOURNAL OF CARDIOLOGY
英文刊物名称: INTERNATIONAL JOURNAL OF CARDIOLOGY
论文全文:
英文论文全文:
全文链接:
其它备注:
英文其它备注:
学科: Cardiovascular System & Cardiology
英文学科: Cardiovascular System & Cardiology
影响因子: 4.036
第一作者所在部门:
英文第一作者所在部门:
论文出处:
英文论文出处:
论文类别: Article
英文论文类别: Article
参与作者:
英文参与作者:
 
2014 中国科学院上海生命科学研究院 版权所有