Ghrelin Could be a Candidate for the Prevention of In-Stent Restenosis

被引:12
作者
Shu, Z. W. [1 ,2 ]
Yu, M. [1 ,2 ]
Chen, X. J. [1 ]
Tan, X. R. [1 ]
机构
[1] Shantou Univ, Coll Med, Affiliated Hosp 1, Dept Cardiol, Shantou 515041, Guangdong, Peoples R China
[2] Shantou Univ, Coll Med, Affiliated Hosp 1, Mol Biol Lab, Shantou 515041, Guangdong, Peoples R China
关键词
Ghrelin; Inflammation; Proliferation; Endothelial function; Antithrombosis; In-stent restenosis; SMOOTH-MUSCLE-CELLS; AORTIC ENDOTHELIAL-CELLS; RATS; PROLIFERATION; ACTIVATION; EXPRESSION; HORMONE; LEPTIN; ERK1/2; ANGIOGENESIS;
D O I
10.1007/s10557-013-6453-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Percutaneous coronary intervention is a revolutionary treatment for ischemic heart disease, but in-stent restenosis (ISR) remains a clinical challenge. Inflammation, smooth muscle proliferation, endothelial function impairment, and local thrombosis have been identified as the main mechanisms for ISR. Considering the multifactorial mechanisms of ISR, a novel therapeutic agent with multiple bioactivities is required. Ghrelin is a novel gut-brain peptide predominantly produced by the stomach, and has been shown to play a role in various cardiovascular activities, such as increasing myocardial contractility, improving cardiac output, and inhibiting ventricular remodeling, as well as attenuating cardiac ischemia-reperfusion injury. Recent studies have demonstrated that ghrelin effectively inhibits vascular inflammation and vascular smooth muscle cell proliferation, repairs endothelial cells, promotes vascular endothelial function, inhibits platelet aggregation, and exerts antithrombotic effects. These findings suggest that ghrelin may be an innovative therapeutic candidate for the prevention and treatment of ISR.
引用
收藏
页码:309 / 314
页数:6
相关论文
共 46 条
  • [1] Ahluwalia A, 2009, J PHYSIOL PHARMACOL, V60, P29
  • [2] Protective role of ghrelin against carbon tetrachloride (CCl4)-induced coagulation disturbances in rats
    Arici, Omer Faruk
    Cetin, Nazmi
    [J]. REGULATORY PEPTIDES, 2011, 166 (1-3) : 139 - 142
  • [3] Ghrelin and des-acyl ghrelin inhibit cell death in cardiomyocytes and endothelial cells through ERK1/2 and PI 3-kinase/AKT
    Baldanzi, G
    Filigheddu, N
    Cutrupi, S
    Catapano, F
    Bonissoni, S
    Fubini, A
    Malan, D
    Baj, G
    Granata, R
    Broglio, F
    Papotti, M
    Surico, N
    Bussolino, F
    Isgaard, J
    Deghenghi, R
    Sinigaglia, F
    Prat, M
    Muccioli, G
    Ghigo, E
    Graziani, A
    [J]. JOURNAL OF CELL BIOLOGY, 2002, 159 (06) : 1029 - 1037
  • [4] Protective effects of ghrelin on ischemia/reperfusion injury in the isolated rat heart
    Chang, L
    Ren, YS
    Liu, XH
    Li, WG
    Yang, JH
    Geng, B
    Weintraub, NL
    Tang, CS
    [J]. JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2004, 43 (02) : 165 - 170
  • [5] PDGF-D contributes to neointimal hyperplasia in rat model of vessel injury
    Chen, JZ
    Han, Y
    Lin, CX
    Zhen, YS
    Song, XD
    Teng, SY
    Chen, C
    Chen, Y
    Zhang, YH
    Hui, RT
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2005, 329 (03) : 976 - 983
  • [6] Anti-Inflammatory Activity of Ghrelin in Human Carotid Artery Cells
    Chow, Kevin B. S.
    Cheng, Christopher H. K.
    Wise, Helen
    [J]. INFLAMMATION, 2009, 32 (06) : 402 - 409
  • [7] Ghrelin inhibits FGF-2-mediated angiogenesis in vitro and in vivo
    Conconi, MT
    Nico, B
    Guidolin, D
    Baiguera, S
    Spinazzi, R
    Rebuffat, P
    Malendowicz, LK
    Vacca, A
    Carraro, G
    Parnigotto, PP
    Nussdorfer, GG
    Ribatti, D
    [J]. PEPTIDES, 2004, 25 (12) : 2179 - 2185
  • [8] Deng B, 2010, CHIN J ARTERIOSCLER, V18, P487
  • [9] Deng Bin, 2010, Zhong Nan Da Xue Xue Bao Yi Xue Ban, V35, P1037, DOI 10.3969/j.issn.1672-7347.2010.10.003
  • [10] Molecular signatures determining coronary artery and saphenous vein smooth muscle cell phenotypes - Distinct responses to stimuli
    Deng, DXF
    Spin, JM
    Tsalenko, A
    Vailaya, A
    Ben-Dor, A
    Yakhini, Z
    Tsao, P
    Bruhn, L
    Quertermous, T
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2006, 26 (05) : 1058 - 1065