Cyclophilin A - Promising New Target in Cardiovascular Therapy

被引:74
作者
Satoh, Kimio [1 ,2 ,3 ]
Shimokawa, Hiroaki
Berk, Bradford C. [2 ,3 ]
机构
[1] Tohoku Univ, Grad Sch Med, Dept Cardiovasc Med, Aoba Ku, Sendai, Miyagi 9808574, Japan
[2] Univ Rochester, Sch Med & Dent, Dept Med, Rochester, NY 14642 USA
[3] Univ Rochester, Sch Med & Dent, Inst Med, Rochester, NY USA
关键词
Immunophilin; Matrix metalloproteinase; Reactive oxygen species; Remodeling; Vasculature; INDUCED PULMONARY-HYPERTENSION; ABDOMINAL-AORTIC-ANEURYSM; SMOOTH-MUSCLE-CELLS; METALLOPROTEINASE INDUCER EMMPRIN; II-INDUCED ATHEROSCLEROSIS; RHO-KINASE INHIBITOR; OXIDATIVE STRESS; BINDING-PROTEIN; ENDOTHELIAL DYSFUNCTION; ERYTHROPOIETIN RECEPTOR;
D O I
10.1253/circj.CJ-10-0904
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cyclophilin A (CyPA) has been studied as a multifunctional protein that is upregulated in a variety of inflammatory conditions, such as rheumatoid arthritis, autoimmune disease, and cancer. CyPA has been classified as an immunophilin and has a variety of intracellular functions, including intracellular signaling, protein trafficking, and the regulation of other proteins activity. Besides its intracellular functions, CyPA is a secreted molecule that has a physiological and pathological role in cardiovascular diseases, making it a potential biomarker and mediator in cardiovascular diseases, such as vascular stenosis, atherosclerosis, and abdominal aortic aneurysms. (Circ J 2010; 74: 2249-2256)
引用
收藏
页码:2249 / 2256
页数:8
相关论文
共 104 条
[1]   Long-term treatment with a Rho-kinase inhibitor improves monocrotaline-induced fatal pulmonary hypertension in rats [J].
Abe, K ;
Shimokawa, H ;
Morikawa, K ;
Uwatoku, T ;
Oi, K ;
Matsumoto, Y ;
Hattori, T ;
Nakashima, Y ;
Kaibuchi, K ;
Sueishi, K ;
Takeshita, A .
CIRCULATION RESEARCH, 2004, 94 (03) :385-393
[2]   NADPH oxidase signaling and cardiac myocyte function [J].
Akki, Ashwin ;
Zhang, Min ;
Murdoch, Colin ;
Brewer, Alison ;
Shah, Ajay M. .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2009, 47 (01) :15-22
[4]   DIFFERENTIAL ACTIVATION OF MITOGEN-ACTIVATED PROTEIN-KINASES BY H2O2 AND O-2(-) IN VASCULAR SMOOTH-MUSCLE CELLS [J].
BAAS, AS ;
BERK, BC .
CIRCULATION RESEARCH, 1995, 77 (01) :29-36
[5]   Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death [J].
Baines, CP ;
Kaiser, RA ;
Purcell, NH ;
Blair, NS ;
Osinska, H ;
Hambleton, MA ;
Brunskill, EW ;
Sayen, MR ;
Gottlieb, RA ;
Dorn, GW ;
Robbins, J ;
Molkentin, JD .
NATURE, 2005, 434 (7033) :658-662
[6]  
BERGSMA DJ, 1991, J BIOL CHEM, V266, P23204
[7]   Vascular smooth muscle growth: Autocrine growth mechanisms [J].
Berk, BC .
PHYSIOLOGICAL REVIEWS, 2001, 81 (03) :999-1030
[8]   VASOCONSTRICTION - A NEW ACTIVITY FOR PLATELET-DERIVED GROWTH-FACTOR [J].
BERK, BC ;
ALEXANDER, RW ;
BROCK, TA ;
GIMBRONE, MA ;
WEBB, RC .
SCIENCE, 1986, 232 (4746) :87-90
[9]  
BIERER BE, 1994, CHEM IMMUNOL, V59, P128
[10]   Angiotensin II-accelerated atherosclerosis and aneurysm formation is attenuated in osteopontin-deficient mice [J].
Bruemmer, D ;
Collins, AR ;
Noh, G ;
Wang, W ;
Territo, M ;
Arias-Magallona, S ;
Fishbein, MC ;
Blaschke, F ;
Kintscher, U ;
Graf, K ;
Law, RE ;
Hsueh, WA .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (09) :1318-1331