Matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) and transforming growth factor-β (TGF-β) in advanced canine myxomatous mitral valve disease

2014 ◽  
Vol 97 (3) ◽  
pp. 560-567 ◽  
Author(s):  
S.G. Moesgaard ◽  
H. Aupperle ◽  
M.M. Rajamäki ◽  
T. Falk ◽  
C.E. Rasmussen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mitral Valve ◽  
Matrix Metalloproteinases ◽  
Mitral Valve Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Valve Disease ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Tissue Inhibitors

scholarly journals Identification of low circulatory transforming growth factor β-1 in patients with degenerative heart valve disease☆

2010 ◽  
Vol 11 (6) ◽  
pp. 791-793 ◽  
Author(s):  
Saina Attaran ◽  
Roy Sherwood ◽  
Michael Ghosh Dastidar ◽  
Ahmed El-Gamel
Keyword(s):  
Growth Factor ◽  
Heart Valve ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Valve Disease ◽  
Heart Valve Disease

scholarly journals A Genomic Study of Myxomatous Mitral Valve Disease in Cavalier King Charles Spaniels

Animals ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1895
Author(s):  
Arianna Bionda ◽  
Matteo Cortellari ◽  
Mara Bagardi ◽  
Stefano Frattini ◽  
Alessio Negro ◽  
...  
Keyword(s):  
Mitral Valve ◽  
Heart Development ◽  
Mitral Valve Disease ◽  
Transforming Growth Factor ◽  
Valve Disease ◽  
Fixation Index ◽  
Nucleotide Polymorphisms ◽  
Extended Haplotype ◽  
Polygenic Inheritance ◽  
Genomic Study

Cavalier King Charles spaniels (CKCSs) show the earliest onset and the highest incidence of myxomatous mitral valve disease (MMVD). Previous studies have suggested a polygenic inheritance of the disease in this breed and revealed an association with regions on canine chromosomes 13 and 14. Following clinical and echocardiographic examinations, 33 not-directly-related CKCSs were selected and classified as cases (n = 16) if MMVD was present before 5 years of age or as controls (n = 17) if no or very mild MMVD was present after 5 years of age. DNA was extracted from whole blood and genotyped with a Canine 230K SNP BeadChip instrument. Cases and controls were compared with three complementary genomic analyses (Wright’s fixation index—FST, cross-population extended haplotype homozygosity—XP-EHH, and runs of homozygosity—ROH) to identify differences in terms of heterozygosity and regions of homozygosity. The top 1% single-nucleotide polymorphisms (SNPs) were selected and mapped, and the genes were thoroughly investigated. Ten consensus genes were found localized on chromosomes 3-11-14-19, partially confirming previous studies. The HEPACAM2, CDK6, and FAH genes, related to the transforming growth factor β (TGF-β) pathway and heart development, also emerged in the ROH analysis. In conclusion, this work expands the knowledge of the genetic basis of MMVD by identifying genes involved in the early onset of MMVD in CKCSs.

scholarly journals Cardiomyopathy in young adults with classic mitral valve prolapse

2013 ◽  
Vol 24 (4) ◽  
pp. 694-701 ◽  
Author(s):  
Eduard Malev ◽  
Svetlana Reeva ◽  
Lyubov Vasina ◽  
Eugeny Timofeev ◽  
Asiyet Pshepiy ◽  
...  
Keyword(s):  
Young Adults ◽  
Growth Factor ◽  
Mitral Valve ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Mitral Valve Prolapse ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Left Ventricular ◽  
Control Group

AbstractBackground: In some inherited connective tissue diseases with involvement of the cardiovascular system, for example, Marfan syndrome, early impairment of left ventricular function, which have been described as Marfan-related cardiomyopathy has been reported. Our aim was to evaluate the left ventricular function in young adults with mitral valve prolapse without significant mitral regurgitation using two-dimensional strain imaging and to determine the possible role of the transforming growth factor-β pathway in its deterioration. Methods: We studied 78 young adults with mitral valve prolapse without mitral regurgitation in comparison with 80 sex-matched and age-matched healthy individuals. Longitudinal strain and strain rates were defined using spackle tracking. Concentrations of transforming growth factor-β1 and β2 in serum were determined by enzyme-linked immunosorbent assays. Results: In 29 patients, classic relapse was identified with a leaflet thickness of ≥ 5 mm; 49 patients had a non-classic mitral valve prolapse. Despite the similar global systolic function, a significant reduction in global strain was found in the classic group (−15.5 ± 2.9%) compared with the non-classic group (−18.7 ± 3.8; p = 0.0002) and the control group (−19.6 ± 3.4%; p < 0.0001). In young adults with non-classic prolapse, a reduction in longitudinal deformation was detected only in septal segments. Transforming growth factor-β1 and β2 serum levels were elevated in patients with classic prolapse as compared with the control group and the non-classic mitral valve prolapse group. Conclusions: These changes in the deformations may be the first signs of deterioration of the left ventricular function and the existence of primary cardiomyopathy in young adults with mitral valve prolapse, which may be caused by increased transforming growth factor-β signalling.

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