Targeting the angiotensin pathway in idiopathic pulmonary fibrosis

被引:8
作者
Antoniu, Sabina A. [1 ]
机构
[1] Univ Med & Pharm Gr T Popa Iasi, Romania Div Pulm Dis, Pulm Dis Univ Hosp, Iasi 700115, Romania
关键词
angiotensin II type 1 receptors (AT1); belomycin-induced pulmonary fibrosis; olmesartan; PD123319;
D O I
10.1517/14728220802515459
中图分类号
R9 [药学];
学科分类号
1007 [药学];
摘要
Background: The angiotensin pathway is involved in the pathogenesis of many fibrotic diseases and in idiopathic pulmonary fibrosis an innate overexpression of angiotensin II, a potent TGF-beta 1 inductor has been demonstrated. Angiotensin II therapeutic blockade could be therefore a promising antifibrotic approach. Objective: Discussion of the results of a preclinical study assessing the antifibrotic efficacy of olmesartan and PD123319 in an experimental lung fibrosis [1]. Methods/results: This study demonstrated that in belomycin-induced pulmonary fibrosis both compounds had significant anti-inflammatory and antifibrotic activities. Conclusion: Targeting the angiotensin pathway with specific blocking agents could represent a promising antifibrotic treatment.
引用
收藏
页码:1587 / 1590
页数:4
相关论文
共 14 条
[1]
Chronic blockade of angiotensin II AT1-receptors increased cell-to-cell communication, reduced fibrosis and improved impulse propagation in the failing heart [J].
De Mello, Walmor C. ;
Specht, Philip .
JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM, 2006, 7 (04) :201-205
[2]
ANGIOTENSIN-II STIMULATES EXTRACELLULAR-MATRIX PROTEIN-SYNTHESIS THROUGH INDUCTION OF TRANSFORMING GROWTH-FACTOR-BETA EXPRESSION IN RAT GLOMERULAR MESANGIAL CELLS [J].
KAGAMI, S ;
BORDER, WA ;
MILLER, DE ;
NOBLE, NA .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (06) :2431-2437
[3]
Angiotensin II antagonism fails to ameliorate bleomycin-induced pulmonary fibrosis in mice [J].
Keogh, KA ;
Standing, J ;
Kane, GC ;
Terzic, A ;
Limper, AH .
EUROPEAN RESPIRATORY JOURNAL, 2005, 25 (04) :708-714
[4]
ANGIOTENSIN-II STIMULATES THE AUTOCRINE PRODUCTION OF TRANSFORMING GROWTH-FACTOR-BETA-1 IN ADULT-RAT CARDIAC FIBROBLASTS [J].
LEE, AA ;
DILLMANN, WH ;
MCCULLOCH, AD ;
VILLARREAL, FJ .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (10) :2347-2357
[5]
Angiotensin converting enzyme-2 is protective but downregulated in human and experimental lung fibrosis [J].
Li, Xiaopeng ;
Molina-Molina, Maria ;
Abdul-Hafez, Amal ;
Uhal, Victor ;
Xaubet, Antonio ;
Uhal, Bruce D. .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2008, 295 (01) :L178-L185
[6]
Essential roles for angiotensin receptor AT1a in bleomycin-induced apoptosis and lung fibrosis in mice [J].
Li, XP ;
Rayford, H ;
Uhal, BD .
AMERICAN JOURNAL OF PATHOLOGY, 2003, 163 (06) :2523-2530
[7]
Losartan attenuates bleomycin induced lung fibrosis by increasing prostaglandin E2 synthesis [J].
Molina-Molina, M. ;
Serrano-Mollar, A. ;
Bulbena, O. ;
Fernandez-Zabalegui, L. ;
Closa, D. ;
Marin-Arguedas, A. ;
Torrego, A. ;
Mullol, J. ;
Picado, C. ;
Xaubet, A. .
THORAX, 2006, 61 (07) :604-610
[8]
Reduction of bleomycin induced lung fibrosis by candesartan cilexetil, an angiotension II type 1 receptor antagonist [J].
Otsuka, M ;
Takahashi, H ;
Shiratori, M ;
Chiba, H ;
Abe, S .
THORAX, 2004, 59 (01) :31-37
[9]
Angiotensin receptor subtype AT1 mediates alveolar epithelial cell apoptosis in response to ANG II [J].
Papp, M ;
Li, XP ;
Zhuang, JJ ;
Wang, RQ ;
Uhal, BD .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2002, 282 (04) :L713-L718
[10]
Selman Moises, 2006, Proc Am Thorac Soc, V3, P364, DOI 10.1513/pats.200601-003TK