New perspectives on endothelin-1 in atherosclerosis and diabetes mellitus

被引：109

作者：

Pernow, John ^{[1
]}

Shemyakin, Alexey ^{[1
]}

Bohm, Felix ^{[1
]}

机构：

[1] Karolinska Univ Hosp, Dept Med, Cardiol Unit, Karolinska Inst, S-17176 Stockholm, Sweden

来源：

LIFE SCIENCES | 2012年 / 91卷 / 13-14期

关键词：

Endothelium; Vasoconstriction; Inflammation; Oxidative stress; Receptors; Glucose; Insulin resistance; INSULIN-RECEPTOR SUBSTRATE-1; NITRIC-OXIDE SYNTHASE; HUMAN CORONARY-ARTERY; TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE-CELLS; ANGIOTENSIN-II; ETA-RECEPTOR; ENDOGENOUS ENDOTHELIN; SUPEROXIDE-PRODUCTION; GLUCOSE-UPTAKE;

D O I：

10.1016/j.lfs.2012.03.029

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Endothelin-1 (ET-1) is a vasoconstrictor, proinflammatory and proliferative endothelial cell-derived peptide that is of significant importance in the regulation of vascular function. It is involved in the development of endothelial dysfunction including important interactions with nitric oxide. The expression and functional effects of ET-1 and its receptors are markedly altered during development of cardiovascular disease. Increased production of ET-1 and its receptors mediate many pathophysiological events contributing to the development of atherosclerosis and vascular complications in diabetes mellitus. The present review focuses on the pathophysiological role of ET-1 and the potential importance of ET receptors as a therapeutic target for treatment of these conditions. (c) 2012 Elsevier Inc. All rights reserved.

引用

页码：507 / 516

页数：10

共 136 条

[61] ENDOTHELIN-1 IS AN AUTOCRINE PARACRINE FACTOR IN THE MECHANISM OF ANGIOTENSIN-II-INDUCED HYPERTROPHY IN CULTURED RAT CARDIOMYOCYTES [J].

ITO, H ;

HIRATA, Y ;

ADACHI, S ;

TANAKA, M ;

TSUJINO, M ;

KOIKE, A ;

NOGAMI, A ;

MARUMO, F ;

HIROE, M .

JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (01) :398-403

[62]

Iwasa Naoko, 2010, Kobe J Med Sci, V56, pE85

[63] Increased immunoreactivity of endothelin-1 and endothelin B receptor in human atherosclerotic lesions. A possible role in atherogenesis [J].

Iwasa, S ;

Fan, JL ;

Shimokama, T ;

Nagata, M ;

Watanabe, T .

ATHEROSCLEROSIS, 1999, 146 (01) :93-100

[64] Endothelial dysfunction in insulin resistance and type 2 diabetes [J].

Jansson, P.-A. .

JOURNAL OF INTERNAL MEDICINE, 2007, 262 (02) :173-183

[65] Endothelin-l modulates insulin signaling through phosphatidylinositol 3-kinase pathway in vascular smooth muscle cells [J].

Jiang, ZY ;

Zhou, QL ;

Chatterjee, A ;

Feener, EP ;

Myers, MG ;

White, MF ;

King, GL .

DIABETES, 1999, 48 (05) :1120-1130

[66]

Kalani Majid, 2008, Diabetes Care, V31, pe56, DOI 10.2337/dc08-0409

[67] Endothelin-1-induced impairment of endothelium-dependent relaxation in aortas isolated from controls and diabetic rats [J].

Kamata, K ;

Kanie, N ;

Matsumoto, T ;

Kobayashi, T .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2004, 44 :S186-S190

[68] Effects of chronic administration of the novel endothelin antagonist J-104132 on endothelial dysfunction in streptozotocin-induced diabetic rat [J].

Kanie, N ;

Kamata, K .

BRITISH JOURNAL OF PHARMACOLOGY, 2002, 135 (08) :1935-1942

[69] INCREASED PLASMA ENDOTHELIN IN NIDDM PATIENTS WITH RETINOPATHY [J].

KAWAMURA, M ;

OHGAWARA, H ;

NARUSE, M ;

SUZUKI, N ;

IWASAKI, N ;

NARUSE, K ;

HORI, S ;

DEMURA, H ;

OMORI, Y .

DIABETES CARE, 1992, 15 (10) :1396-1397

[70] Cardiomyocyte-specific endothelin A receptor knockout mice have normal cardiac function and an unaltered hypertrophic response to angiotensin II and isoproterenol [J].

Kedzierski, RM ;

Grayburn, PA ;

Kisanuki, YY ;

Williams, CS ;

Hammer, RE ;

Richardson, JA ;

Schneider, MD ;

Yanagisawa, M .

MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (22) :8226-8232

← 2 3 4 5 6 7 8 9 10 11 →