Abstract:
:Morphogenesis and developmental remodeling of cardiovascular tissues involve coordinated regulation of cell proliferation and apoptosis. In the heart, clear evidence points toward focal apoptosis as a contributor to development of the embryonic outflow tract, cardiac valves, conducting system, and the developing coronary vasculature. Apoptosis in the heart is likely regulated by survival and death signals that are also present in many other tissues. Cell type-specific regulation may be superimposed on general cell death/survival machinery through tissue-specific transcriptional pathways. In the vasculature, apoptosis almost certainly contributes to developmental vessel regression, and it is of proven importance in remodeling of arterial structure in response to local changes in hemodynamics. Physical forces, growth factors, and extracellular matrix drive vascular cell survival pathways, and considerable evidence points to local nitric oxide production as an important but complex regulator of vascular cell death. In both the heart and vasculature, progress has been impeded by inadequate information concerning the incidence of apoptosis, its relative importance compared with the diverse cell behaviors that remodel developing tissues, and by our primitive knowledge concerning regulation of cell death in these tissues. However, tools are now available to better understand apoptosis in normal and abnormal development of cardiovascular structures, and a framework has been established that should lead to considerable progress in the coming years.
journal_name
Circ Resjournal_title
Circulation researchauthors
Fisher SA,Langille BL,Srivastava Ddoi
10.1161/01.res.87.10.856subject
Has Abstractpub_date
2000-11-10 00:00:00pages
856-64issue
10eissn
0009-7330issn
1524-4571journal_volume
87pub_type
杂志文章,评审abstract::We have previously demonstrated that urokinase-type plasminogen activator (uPA) is highly expressed in the aneurysmal segment of the abdominal aorta (AAA) in apolipoprotein E-deficient (apoE-/-) mice treated with angiotensin II (Ang II). In the present study, we tested the hypothesis that uPA is essential for AAA form...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000061571.49375.E1
更新日期:2003-03-21 00:00:00
abstract::To investigate the effect of lactate, pyruvate, and glucose on the endogenous levels of lipids in the normoxic, ischemic, and reperfused myocardium, isolated working rat hearts were exposed to various grades of ischemic insult (15, 30, or 45 minutes). Glucose was present as the basal substrate in the perfusion medium,...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.72.1.176
更新日期:1993-01-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.50.2.294
更新日期:1982-02-01 00:00:00
abstract::The contractile response of the aged adult heart to beta-adrenergic stimulation is known to be reduced compared with the young adult heart. Since endogenous adenosine exerts an antiadrenergic action in the heart, this study was undertaken to determine if the basal endogenous level of myocardial adenosine increases wit...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.66.5.1381
更新日期:1990-05-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.61.2.256
更新日期:1987-08-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000217342.83731.89
更新日期:2006-04-14 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.88.3.319
更新日期:2001-02-16 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.117.305925
更新日期:2015-07-31 00:00:00
abstract::Complete knowledge of myocardial structure, metabolism, and function is crucial to understanding the response of the heart to injury such as ischemia. Increasingly, this type of knowledge is required at multiple levels, from that of the isolated myocyte to the functioning organism, to provide basic scientists and clin...
journal_title:Circulation research
pub_type: 杂志文章,评审
doi:10.1161/01.RES.0000103863.40055.E8
更新日期:2003-12-12 00:00:00
abstract:RATIONALE:Lymphatic vessels in the respiratory tract normally mature into a functional network during the neonatal period, but under some pathological conditions they can grow as enlarged, dilated sacs that result in the potentially lethal condition of pulmonary lymphangiectasia. OBJECTIVE:We sought to determine wheth...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.114.303119
更新日期:2014-02-28 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.42.2.263
更新日期:1978-02-01 00:00:00
abstract::Vagal afferents from the cardiopulmonary region exert a tonic inhibition on the vasomotor center. This is demonstrated by constriction of systemic resistance and splanchnic capacitance vessels and by increased output of renin when the vagi are cut or blocked. In dogs, removal or selective denervation of organs showed ...
journal_title:Circulation research
pub_type: 杂志文章,评审
doi:10.1161/01.res.38.6.2
更新日期:1976-06-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.74.4.641
更新日期:1994-04-01 00:00:00
abstract::A period of prolonged vasodilation follows flow-restricted exercise of skeletal muscle. We tested the hypothesis that adenosine participates in mediating this vascular response. Vascularly isolated, anterior calf muscles of anesthetized dogs were stimulated to contract at a rate of 4 twitches/sec. Blood flow was held ...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.44.6.759
更新日期:1979-06-01 00:00:00
abstract::The mechanisms underlying the blunted contractile response to beta-adrenergic receptor (beta-AR) stimulation in heart failure (HF) are incompletely understood, especially with regard to beta-AR subtype-specific regulation of L-type Ca2+ channels. We evaluated the impact of HF induced by pacing tachycardia on beta-AR r...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000181160.31851.05
更新日期:2005-09-16 00:00:00
abstract::In patients with congestive heart failure, skeletal muscle is characterized by a smaller proportion of slow-twitch oxidative fibers and reduced oxidative enzyme activity. However, whether these changes result from disuse or occur as a direct consequence of heart failure is unresolved. To address this issue, 18 rats wi...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.79.1.128
更新日期:1996-07-01 00:00:00
abstract::Muscle ring finger (MuRF) proteins have been implicated in transmitting mechanical forces to cell signaling pathways through their interactions with the giant protein titin. Recent evidence has linked mechanically-induced stimuli with the control of serum response factor activity and localization through MuRF2. This o...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000259559.48597.32
更新日期:2007-03-02 00:00:00
abstract::Ventricular arrhythmias that accompany myocardial infarction in dogs may be secondary to the altered electrophysiological properties of the subendocardial Purkinje fibers that survive 24 hours after the coronary occlusion. To better understand the ionic mechanisms that underlie the altered electrical activity of these...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.65.4.955
更新日期:1989-10-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.87.3.201
更新日期:2000-08-04 00:00:00
abstract::We report the hemodynamic parameters of stage 18, 21, 24, and 27 chick embryos (from 3 to 5 days of incubation). Dorsal aortic blood velocity and mean vitelline artery blood pressure are measured with a 20 MHz pulsed-Doppler meter and servo-null pressure system respectively. We also measure heart rate, dorsal aortic d...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.51.6.810
更新日期:1982-12-01 00:00:00
abstract::We investigated the effects of streptozotocin-induced diabetes on atrial natriuretic peptide (ANP) synthesis, hemodynamic parameters, blood volume, and histopathology, as well as the reversibility of such effects with insulin therapy in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). The biatrial A...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.67.4.803
更新日期:1990-10-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.117.305784
更新日期:2015-07-03 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.86.4.448
更新日期:2000-03-03 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.57.2.319
更新日期:1985-08-01 00:00:00
abstract:RATIONALE:Thioredoxin (Trx)1 inhibits pathological cardiac hypertrophy. MicroRNAs (miRNAs) are small noncoding RNAs that downregulate posttranscriptional expression of target molecules. OBJECTIVES:We investigated the role of miRNAs in mediating the antihypertrophic effect of Trx1 on angiotensin II (Ang II)-induced car...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/CIRCRESAHA.110.228437
更新日期:2011-02-04 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
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更新日期:1997-07-01 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
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更新日期:1979-08-01 00:00:00
abstract::We tested the hypothesis that TNF-alpha induces early-onset endothelial adhesivity toward PMN by activating the constitutive endothelial cell surface ICAM-1, the beta2-integrin (CD11/CD18) counter-receptor. Stimulation of human pulmonary artery endothelial cells with TNF-alpha resulted in phosphorylation of ICAM-1 wit...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.RES.0000072971.88704.CB
更新日期:2003-05-30 00:00:00
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journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/hh0102.103221
更新日期:2002-01-11 00:00:00
abstract::Endothelin-1 (ET-1) and endothelin-3 (ET-3) produced positive inotropic effects on electrically stimulated left atria and increased the frequency of spontaneously beating right atria of adult rats. The potency of the inotropic effect of ET-1 was greater than that of ET-3, but the potencies of the chronotropic effects ...
journal_title:Circulation research
pub_type: 杂志文章
doi:10.1161/01.res.69.4.918
更新日期:1991-10-01 00:00:00