Is endothelial progenitor cell dysfunction involved in altered angiogenic processes in patients with hypertension?
Hypertension represents one of the most frequent modifiable risk factors for cardiovascular disease (CVD). Despite the arrival of novel antihypertensive drugs and progress in primary prevention and screening, the improvement of blood pressure control does not similarly reduce the incidence of end-or...
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| Published in: | Current hypertension reports Vol. 6; no. 1; pp. 51 - 54 |
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01-02-2004
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| Abstract | Hypertension represents one of the most frequent modifiable risk factors for cardiovascular disease (CVD). Despite the arrival of novel antihypertensive drugs and progress in primary prevention and screening, the improvement of blood pressure control does not similarly reduce the incidence of end-organ damage associated with hypertension. Recently, the concept of reduced angiogenesis as a new CVD risk factor has gained the interest of an increasing number of investigators in the field. Indeed, pharmacologic and stem cell-based strategies aimed to induce angiogenesis seem to improve the course of ischemic vascular disease. However, few to no reports have studied the possible therapeutic potential of angiogenesis in essential hypertension. In this review, we discuss the potential involvement of endothelial progenitor cells in modulating angiogenesis and their putative therapeutic role in improving capillary rarefaction and arterial stiffness in essential hypertensive patients. |
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| AbstractList | Hypertension represents one of the most frequent modifiable risk factors for cardiovascular disease (CVD). Despite the arrival of novel antihypertensive drugs and progress in primary prevention and screening, the improvement of blood pressure control does not similarly reduce the incidence of end-organ damage associated with hypertension. Recently, the concept of reduced angiogenesis as a new CVD risk factor has gained the interest of an increasing number of investigators in the field. Indeed, pharmacologic and stem cell-based strategies aimed to induce angiogenesis seem to improve the course of ischemic vascular disease. However, few to no reports have studied the possible therapeutic potential of angiogenesis in essential hypertension. In this review, we discuss the potential involvement of endothelial progenitor cells in modulating angiogenesis and their putative therapeutic role in improving capillary rarefaction and arterial stiffness in essential hypertensive patients. Hypertension represents one of the most frequent modifiable risk factors for cardiovascular disease (CVD). Despite the arrival of novel antihypertensive drugs and progress in primary prevention and screening, the improvement of blood pressure control does not similarly reduce the incidence of end-organ damage associated with hypertension. Recently, the concept of reduced angiogenesis as a new CVD risk factor has gained the interest of an increasing number of investigators in the field. Indeed, pharmacologic and stem cell-based strategies aimed to induce angiogenesis seem to improve the course of ischemic vascular disease. However, few to no reports have studied the possible therapeutic potential of angiogenesis in essential hypertension. In this review, we discuss the potential involvement of endothelial progenitor cells in modulating angiogenesis and their putative therapeutic role in improving capillary rarefaction and arterial stiffness in essential hypertensive patients.[PUBLICATION ABSTRACT] |
| Author | Loomans, Cindy J M Dao, Huy H van Zonneveld, Anton J Rabelink, Ton J |
| Author_xml | – sequence: 1 givenname: Cindy J M surname: Loomans fullname: Loomans, Cindy J M organization: Department of Vascular Medicine, University Medical Center of Utrecht, G02.228, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands – sequence: 2 givenname: Huy H surname: Dao fullname: Dao, Huy H – sequence: 3 givenname: Anton J surname: van Zonneveld fullname: van Zonneveld, Anton J – sequence: 4 givenname: Ton J surname: Rabelink fullname: Rabelink, Ton J |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/14972094$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_thromres_2014_12_006 crossref_primary_10_1016_j_jash_2011_11_003 crossref_primary_10_1186_1755_1536_5_13 crossref_primary_10_1042_CS20100429 crossref_primary_10_1152_ajpendo_00026_2011 crossref_primary_10_1161_01_HYP_0000249510_20326_72 crossref_primary_10_1016_j_clinbiochem_2010_06_020 crossref_primary_10_14814_phy2_12358 crossref_primary_10_1016_j_cca_2007_09_026 crossref_primary_10_1586_erc_10_105 crossref_primary_10_1097_MAJ_0b013e3181c6a968 crossref_primary_10_1291_hypres_29_1047 crossref_primary_10_1097_TA_0b013e3181e772b0 |
| Cites_doi | 10.1038/sj.jhh.1001470 10.1073/pnas.181177898 10.1126/science.275.5302.964 10.1016/S0895-7061(03)00052-9 10.1172/JCI200113131 10.1093/cvr/27.6.951 10.1161/01.RES.0000083812.30141.74 10.1161/01.STR.0000076013.00240.B0 10.1161/01.CIR.0000043246.74879.CD 10.2174/1381612033454540 10.1097/00004872-200202000-00017 10.1161/01.HYP.34.4.655 10.1038/sj.jhh.1001454 10.1161/hc1002.105135 10.1172/JCI8296 10.1016/S0140-6736(02)09670-8 10.1182/blood.V92.2.362 10.1182/blood-2003-01-0223 10.1161/hh1301.093953 10.1161/01.CIR.0000018166.84319.55 10.1097/00004872-199816110-00001 10.1006/jsbi.1996.3835 10.1172/JCI200113152 10.1161/01.HYP.37.2.381 10.1161/01.CIR.0000039526.42991.93 10.1172/JCI119354 10.1161/01.CIR.0000074242.66719.4A 10.1161/01.RES.85.3.221 10.1016/S1050-1738(03)00077-X 10.1161/01.CIR.99.23.3043 10.1038/nm0903-1109 10.1056/NEJMoa022287 10.1172/JCI9087 10.1093/ndt/17.10.1728 10.1016/S0002-9440(10)65282-0 10.1016/S1050-1738(01)00152-9 |
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| Title | Is endothelial progenitor cell dysfunction involved in altered angiogenic processes in patients with hypertension? |
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