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קהילה:
אסיף מאגר המחקר החקלאי
פותח על ידי קלירמאש פתרונות בע"מ -
Inhibition of fibrosis and improvement of function of the myopathic hamster cardiac muscle by halofuginone
Year:
2014
Authors :
גנין, אולגה
;
.
לוי, אשרת
;
.
פינס, מרק
;
.
Volume :
20
Co-Authors:
Fromes, Y., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Bouyon, S., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Nagi, S., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Roussel, V., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Genin, O., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Levi, O., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Pines, M., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Facilitators :
From page:
2351
To page:
2383
(
Total pages:
33
)
Abstract:
BACKGROUND: Heart injury, which results from various causes, leads to a common final pathway of pathological remodeling and fibrosis that causes heart failure. OBJECTIVES: To evaluated the efficacy of halofuginone in reducing fibrosis and improving cardiac function in the myopathic hamster strain CHF147 that develop a cardiomyopathy which evolves into heart failure with a major increase in fibrosis. METHODS: Echocardiography and surface ECG were assessed with and without halofuginone treatment. Cardiac biopsies were stained for collagen and immunostained for pSmad3, collagen triple-helix repeat containing 1 (cthrc1). Collagen α1(I) was evaluated by in situ hybridization. Myofibroblasts number was assessed by immunostaining for collagen cross-linking enzyme. RESULTS: Halofuginone treatment resulted in a major reduction in cardiac collagen and cthrc1 levels that was associated with prevention and deceleration of the impairment of left ventricular function. Halofuginone reduced the number of myofibroblasts and reduced the number of nuclei with pSmad3 downstream of the TGFβ signaling. CONCLUSIONS: Halofuginone that inhibited cardiac collagen synthesis and improved cardiac function meets the criteria for a potential novel antifibrotic therapy for patients with cardiac fibrosis of various etiologies.
Note:
Related Files :
animal cell
animal experiment
animal model
animal tissue
gene expression
heart failure
Male
transforming growth factor beta
עוד תגיות
תוכן קשור
More details
DOI :
Article number:
0
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
28682
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:41
Scientific Publication
Inhibition of fibrosis and improvement of function of the myopathic hamster cardiac muscle by halofuginone
20
Fromes, Y., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Bouyon, S., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Nagi, S., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Roussel, V., UPMC, Institut de Myologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France
Genin, O., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Levi, O., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Pines, M., Institute of Animal Sciences, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Inhibition of fibrosis and improvement of function of the myopathic hamster cardiac muscle by halofuginone
BACKGROUND: Heart injury, which results from various causes, leads to a common final pathway of pathological remodeling and fibrosis that causes heart failure. OBJECTIVES: To evaluated the efficacy of halofuginone in reducing fibrosis and improving cardiac function in the myopathic hamster strain CHF147 that develop a cardiomyopathy which evolves into heart failure with a major increase in fibrosis. METHODS: Echocardiography and surface ECG were assessed with and without halofuginone treatment. Cardiac biopsies were stained for collagen and immunostained for pSmad3, collagen triple-helix repeat containing 1 (cthrc1). Collagen α1(I) was evaluated by in situ hybridization. Myofibroblasts number was assessed by immunostaining for collagen cross-linking enzyme. RESULTS: Halofuginone treatment resulted in a major reduction in cardiac collagen and cthrc1 levels that was associated with prevention and deceleration of the impairment of left ventricular function. Halofuginone reduced the number of myofibroblasts and reduced the number of nuclei with pSmad3 downstream of the TGFβ signaling. CONCLUSIONS: Halofuginone that inhibited cardiac collagen synthesis and improved cardiac function meets the criteria for a potential novel antifibrotic therapy for patients with cardiac fibrosis of various etiologies.
Scientific Publication
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