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Query: UMLS:C0018801 (
heart failure
)
72,216
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. For vascular endothelium,
hepatocyte growth factor
(
HGF
) is one of the most potent and specific growth factors, which acts protectively against endothelial dysfunction.
HGF
production is downregulated by angiotensin II (Ang II) in vitro. We hypothesized that
HGF
production is impaired as the result of increased Ang II in patients with congestive heart failure, and that if so, the impaired production should be restored with angiotensin-converting enzyme inhibitors (ACE-I). We studied 16 patients with congestive heart failure caused by previous anterior myocardial infarction in whom left ventricular ejection fraction was 35+/-8% (mean+/-SD). Before and approximately 4 weeks after the treatment with ACE-I, blood samples were collected to measure the levels of
HGF
, Ang II, and brain natriuretic peptide as a biochemical marker for severity of
heart failure
. We also studied 5 control subjects, in whom heparin increased
HGF
production to 48+/-5-fold. However, in patients with
heart failure
,
HGF
response to heparin was significantly attenuated (24+/-5-fold, P<0.05 vs control). Therapy with ACE-I decreased the levels of Ang II and brain natriuretic peptide and restored
HGF
production in response to heparin by 43+/-7-fold, comparable to the control response. In conclusion, impaired
HGF
production was restored after the treatment with ACE-I probably by the mechanism of Ang II suppression. This novel effect of ACE-I may contribute to the clinical improvement in patients with
heart failure
and thereby may have an important therapeutic implication.
...
PMID:Angiotensin-converting enzyme inhibition restores hepatocyte growth factor production in patients with congestive heart failure. 1037 19
A patient with Cowden disease and multiple arteriovenous malformations (AVMs) that resulted in high output
heart failure
is described. Cowden disease is a familial syndrome characterized by endodermal, mesodermal and ectodermal dysplasia causing benign and malignant tumors of the skin, breast, gastrointestinal tract, and thyroid gland. Our patient had gastrointestinal polyposis, a right renal tumor, a left lung tumor, an adenomatous goiter, and typical dermatologic findings such as facial papules, acral keratosis, gingival papillomatosis and hemangiomas. AVMs were observed in the pelvis, cervical vertebra, liver, and right supraclavicular area. Transcatheter embolization was performed 7 times for the pelvic AVMs, but the effect decreased with repetition and the patient died of
heart failure
2 years after the first embolization. The serum levels of tissue plasminogen activator (t-PA), platelet-derived growth factor (PDGF),
hepatocyte growth factor
(
HGF
), vascular endothelial growth factor (VEGF), and transforming growth factor beta1 were high, suggesting that these angiogenic molecules may play a role in the pathogenesis of AVMs in Cowden disease.
...
PMID:Transcatheter embolization of arteriovenous malformations in Cowden disease. 1047 85
Monitoring of 24-hour ambulatory blood pressure(ABPM), measurements of circulating vasoactive substances and microalbuminuria, and assessment of gene polymorphisms as genetic markers are introduced to detect and evaluate hypertension. Classifications of ABPM based on impact on risks of cardiovascular diseases have been currently available. Plasma level of brain natriuretic peptide(BNP), a cardiac hormone, increases markedly in congestive heart failure, in proportion to its severity, and is evaluated as a potential index of severity of
heart failure
. In addition, serum level of
hepatocyte growth factor
(HGF), a member of endothelium specific growth factors, in hypertension might be useful for evaluating the presence of complications and degree of endothelial dysfunction. In diabetes mellitus, onset of microalbuminuria appeared as an important sign of early nephropathy. There is growing evidence that microalbuminuria is an independent predictor of atherosclerosis and premature death in the general population. Current studies have shown that gene polymorphisms including components of the renin-angiotensin-aldosterone system may be possible genetic markers for hypertension and its associated cardiovascular diseases. Our data suggest positive linkages between hypertension and 4 gene polymorphisms including angiotensinogen Met235Thr, angiotensin converting enzyme I/D, aldosterone synthase CYP11B2 T-344C, and endothelial nitric oxide synthase Glu298Asp in the Aomori population.
...
PMID:[New techniques and laboratory examinations in the detection and evaluation of hypertension]. 1130 25
Impairment of cardiac function in cardiomyopathy has been postulated to be related to decreased blood blow and increased collagen synthesis. Therefore, a therapeutic approach to alter the blood flow or fibrosis directly by means of growth factors may open a new therapeutic concept in dilated cardiomyopathy. From this viewpoint,
hepatocyte growth factor
(
HGF
) is a unique growth factor with antifibrosis and angiogenesis effects. Using the hereditary cardiomyopathic Syrian hamster as a model of genetically determined cardiomyopathy and
heart failure
, the effects of overexpression of
HGF
on fibrosis and microvascular dysfunction were examined.
HGF
gene or control vector was injected by the Hemagglutinating Virus of Japan-liposome method into the anterior heart of cardiomyopathic hamsters (Bio 14.6) under echocardiography once a week, from 12 to 20 weeks of age (total, 8 times). Blood flow, as assessed by a laser Doppler imager score, and the capillary density in hearts, as assessed by alkaline phosphatase staining, were significantly increased in hamsters transfected with
HGF
gene compared with control-vector-transfected hamsters (P<0.01). In contrast, the fibrotic area was significantly decreased in hamsters transfected with
HGF
gene compared with control (P<0.01). Overall, in vivo experiments demonstrated that transfection of
HGF
gene into the myocardium of cardiomyopathic hamsters stimulated blood flow through the induction of angiogenesis and reduction of fibrosis. These results suggest that
HGF
gene transfer may be useful to protect against myocardial injury in cardiomyopathy through its cardioprotective effects such as antifibrosis and angiogenesis actions.
...
PMID:Angiogenesis and antifibrotic action by hepatocyte growth factor in cardiomyopathy. 1210 37
Plasma levels of
hepatocyte growth factor
(
HGF
) are increased within hours of cardiac ischemia/reperfusion in rats, and
HGF
has been shown to be cardioprotective toward acute ischemic injury. Myocardial levels of
HGF
mRNA and protein are increased for several days after myocardial infarction (MI), however, indicating a possible additional protective effect of
HGF
toward the progression of MI to
heart failure
. The purpose of this study was to determine whether
HGF
administration during the time course of endogenous cardiac
HGF
induction would lead to long-term improvement in cardiac function in rats with MI. MI was induced by 2-h occlusion of the left coronary artery, followed by reperfusion.
HGF
was given by intravenous infusion at 0.45 mg/kg/day for 6 days beginning on the day after surgery. Cardiac function and hemodynamic parameters were measured by using indwelling catheters and perivascular flow probes in conscious animals 8 weeks post-MI. Myocardial infarcts were approximately 30% of the left ventricle, and there was no difference in infarct size between the vehicle-treated and
HGF
-treated groups. Compared with untreated sham-operated rats, vehicle-treated MI animals had significantly lower cardiac index and stroke volume index and higher systemic vascular resistance, indicating
heart failure
developed. Treatment with
HGF
caused a significant increase in cardiac index and stroke volume index and a reduction in systemic vascular resistance in rats with MI, restoring these parameters close to those observed in sham-operated control animals. These results provide direct evidence that
HGF
may be of benefit to cardiovascular function in ischemic cardiomyopathy.
...
PMID:Early treatment with hepatocyte growth factor improves cardiac function in experimental heart failure induced by myocardial infarction. 1253 18
The heart is subjected to oxidative stress during various clinical situations, such as ischemia-reperfusion injury and anthracycline chemotherapy. The loss of cardiac myocytes is the major problem in
heart failure
; thus, it is important to protect cardiac myocytes against cell death. Various growth factors, including insulin like growth factor,
hepatocyte growth factor
, endothelin-1, fibroblast growth factor, and transforming growth factor, have been shown to protect the heart against oxidative stress. The mechanism of growth factor-mediated cardioprotection may involve the attenuation of cardiac myocyte apoptosis. The present article summarizes the current knowledge on the molecular mechanisms of growth factor-mediated antiapoptotic signaling in cardiac myocytes. Insulin-like growth factor-1 activates phosphatidylinositol 3' -kinase and extracellular signal-regulated kinase pathways. Recent data showed that GATA-4 might be an important mediator of cardiac myocyte survival by endothelin-1 and
hepatocyte growth factor
. These growth factors, as well as mediators of growth factor-signaling, may be useful in therapeutic strategies against oxidative stress-induced cardiac injury.
...
PMID:Growth factor signaling for cardioprotection against oxidative stress-induced apoptosis. 1458 47
Hepatocyte growth factor
(
HGF
) is a cytokine whose multipotent actions are mediated by c-Met receptor. This review focuses on effects of
HGF
on myocardial infarction (MI) and
heart failure
. Circulating concentrations of
HGF
and myocardial concentrations of
HGF
and c-Met mRNA and protein are substantially increased following acute MI.
HGF
has been shown to be cardioprotective towards acute cardiac ischemia-reperfusion injury. Gene transfection of
HGF
into rat hearts attenuates acute ischemia injury. Administration of
HGF
protein reduces infarct size and increases cardiac performance in a rat model of acute ischemia/reperfusion. In contrast, acute blockade of endogenous
HGF
increases infarct size and mortality. These acute effects of
HGF
appear to be related to angiogenic and anti-apoptotic mechanisms. Recent studies demonstrate that post-MI treatment with
HGF
gene or protein attenuates chronic cardiac remodeling and dysfunction. In rats,
HGF
gene transfer following large MI results in preserved cardiac function and geometry in association with angiogenesis and reduced apoptosis, and treatment with recombinant
HGF
also significantly improves cardiac performance measured 8 weeks after MI. In mice, post-MI
HGF
gene therapy improves cardiac remodeling and dysfunction through hypertrophy of cardiomyocytes, infarct wall thickening, preservation of vessels, and antifibrosis. In addition, gene transfer of
HGF
improves cardiac remodeling, angiogenesis and regional myocardial function in the chronic ischemic myocardium of dogs. Together, these preclinical data highlight the significant acute and chronic cardioprotective effects of
HGF
following ischemic
heart failure
. Clinical trials are needed to investigate the therapeutic potential of
HGF
for postinfarction
heart failure
in humans.
...
PMID:The therapeutic potential of hepatocyte growth factor for myocardial infarction and heart failure. 1532 Jul 61
Hepatocyte growth factor
(
HGF
) is an angiogenic factor upregulated in ischaemic diseases. We measured plasma
HGF
concentration in 26 patients (pts) with stable angina pectoris (SAP) and 16 pts with unstable angina pectoris (UAP).
HGF
levels were significantly higher in pts with UAP compared with pts with SAP (p<0,01), in pts with SAP vs control group (n=38, p<0,01) and in pts with UAP vs control group (p<0,001).
HGF
levels in SAP group correlated with
heart failure
symptoms (p=0,023). There was a trend towards significance between
HGF
and left ventricle ejection fraction (p=0,08) and between
HGF
and VEGF levels in pts with SAP (p=0,08). This study demonstrates that
HGF
plasma levels correlates with SAP symptoms. Pts with SAP and UAP has significantly higher levels of
HGF
comparing with control group.
...
PMID:[Hepatocyte growth factor (HGF) in stable and unstable coronary heart disease]. 1673 98
There is growing evidence of the potential role of
hepatocyte growth factor
(
HGF
) in various cardiovascular diseases. In addition to the beneficial effects of
HGF
in myocardial infarction,
heart failure
, and occlusive peripheral arterial disease, administration of
HGF
effectively suppresses acute and chronic cardiac allograft rejection and autoimmune myocarditis. The present review summarizes recent advances in the utility of
HGF
for heart diseases, especially immune-mediated heart diseases. Possible mechanisms of action in the suppression of T-cell-mediated immunity are also discussed.
...
PMID:Hepatocyte growth factor: Effects on immune-mediated heart diseases. 1683 61
We have developed a mixed ester of hyaluronan with butyric and retinoic acid (HBR) that acted as a novel cardiogenic/vasculogenic agent in human mesenchymal stem cells isolated from bone marrow, dental pulp, and fetal membranes of term placenta (FMhMSCs). HBR remarkably enhanced vascular endothelial growth factor (VEGF), KDR, and
hepatocyte growth factor
(
HGF
) gene expression and the secretion of the angiogenic, mitogenic, and antiapoptotic factors VEGF and
HGF
, priming stem cell differentiation into endothelial cells. HBR also increased the transcription of the cardiac lineage-promoting genes GATA-4 and Nkx-2.5 and the yield of cardiac markerexpressing cells. These responses were notably more pronounced in FMhMSCs. FMhMSC transplantation into infarcted rat hearts was associated with increased capillary density, normalization of left ventricular function, and significant decrease in scar tissue. Transplantation of HBR-preconditioned FMhM-SCs further enhanced capillary density and the yield of human vWF-expressing cells, additionally decreasing the infarct size. Some engrafted, HBR-pretreated FMhMSCs were also positive for connexin 43 and cardiac troponin I. Thus, the beneficial effects of HBR-exposed FMhMSCs may be mediated by a large supply of angiogenic and antiapoptotic factors, and FMhMSC differentiation into vascular cells. These findings may contribute to further development in cell therapy of
heart failure
.
...
PMID:Hyaluronan mixed esters of butyric and retinoic Acid drive cardiac and endothelial fate in term placenta human mesenchymal stem cells and enhance cardiac repair in infarcted rat hearts. 1736 74
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