Saskatoon berry supplementation prevents cardiac remodeling without improving renal disease in an animal model of reno‐cardiac syndrome

2021 ◽  
Vol 45 (10) ◽  
Author(s):  
Pema Raj ◽  
Xavier L. Louis ◽  
Liping Yu ◽  
Yaw L. Siow ◽  
Miyoung Suh ◽  
...  
Keyword(s):  
Animal Model ◽  
Renal Disease ◽  
Cardiac Remodeling ◽  
Cardiac Syndrome

scholarly journals P1274THE CHARACTER OF CARDIAC REMODELING AND VALVE CALCIFICATION IN TYPE 2 DIABETIC PATIENTS WITH END-STAGE RENAL DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Oleksandr Susla ◽  
Mykola Shved ◽  
Zoriana Litovkina ◽  
Svitlana Danyliv ◽  
Anatoliy Gozhenko
Keyword(s):  
Renal Disease ◽  
Cardiac Remodeling ◽  
End Stage Renal Disease ◽  
Systolic Dysfunction ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Stage Renal Disease ◽  
End Stage ◽  
Type 2 Diabetic

Abstract Background and Aims Systematic analysis of cardiac remodeling features in type 2 diabetic patients with end-stage renal disease (ESRD) is important both in stratification of cardiovascular risk and in choice of adequate treatment strategies. The lack of number and fragmentation of studies, the ambiguity of their data regarding the problem of myocardial reconstruction and cardiac valve calcification (CVC) under these conditions have substantiated the need for this study, its relevance and purpose. Method 136 ESRD patients on chronic hemodialysis (HD) were included in this observational cross-sectional study (men, 78; age, 53.9±1.0 years; HD duration, 47.6±4.2 months). The study was performed in accordance with the provisions of the Declaration of Helsinki last revision. Depending on the presence/absence of diabetic nephropathy (DN) all patients were divided into two groups: the 1st one – without DN (n=88); the 2nd one – with DN (n=48). A complete ultrasound examination of the cardiac structure and function including CVC analysis was performed. Data are presented as means±SEM. Mann-Whitney U-test was used for comparison of the quantitative variables, χ2-test – qualitative ones. Results Left ventricular (LV) hypertrophy (93.8 vs. 78.4%, р=0.020) and eccentric hypertrophy (47.9 vs. 28.4%, р=0.023) were diagnosed more often in patients with DN than those without diabetes. Prevalence of pseudonormal and restrictive types of LV diastolic dysfunction (62.5 vs. 28.4%, p<0.001), systolic dysfunction (27.1 vs. 9.1%, p=0.006) and pulmonary hypertension (PH) (64.6 vs. 35.2%, p=0.001) were significant in the 2nd group. CVC (66.6 vs. 38.6%, р=0.002), combined calcification of mitral (MV) and aortal (AV) valves (35.4 vs. 13.6%, p=0.003), stenoses of MV (16.7 vs. 3.4%, p=0.007) and AV (39.6 vs. 15.9%, p=0.004), and insufficiency of MV (66.7 vs. 44.3%, p=0.013) and AV (35.4 vs. 14.8%, p=0.006) were recorded more often in HD patients with DN. LV myocardial mass index (181.0±7.2 vs. 155.0±5.3 g/m2, p=0.001) as well as right ventricle (RV) diameter (2.80±0.09 vs. 2.47±0.04 cm, p=0.003) were also greater in the 2nd group. Conclusion In type 2 diabetic patients with ESRD occurs maladaptive cardiac remodeling with predominance of unfavourable (especially eccentric) types of LV hypertrophy, RV dilatation, PH, severe LV diastolic and systolic dysfunction, and widespread combined calcification of MV and AV with the valve defects. The identification of risk factors for the progression of the pathological reconstruction of myocardium and CVC in HD patients with DN will be the subject of our further research.

scholarly journals Cardioprotective effect of calcineurin inhibition in an animal model of renal disease

2010 ◽  
Vol 32 (15) ◽  
pp. 1935-1945 ◽  
Author(s):  
Giovana S. Di Marco ◽  
Stefan Reuter ◽  
Dominik Kentrup ◽  
Lu Ting ◽  
Liu Ting ◽  
...  
Keyword(s):  
Animal Model ◽  
Renal Disease ◽  
Cardioprotective Effect ◽  
Calcineurin Inhibition

scholarly journals Muscle changes with high-intensity aerobic training in an animal model of renal disease

2019 ◽  
Vol 34 (5) ◽  
Author(s):  
Eliane Barbosa Togoe ◽  
Iandara Schettert Silva ◽  
Juliana Loprete Cury ◽  
Flavia Alessandra Guarnier
Keyword(s):  
Animal Model ◽  
Renal Disease ◽  
High Intensity ◽  
Aerobic Training ◽  
Muscle Changes

scholarly journals Cardiac remodeling and diastolic dysfunction in DahlS.Z-Leprfa/Leprfa rats: a new animal model of metabolic syndrome

2011 ◽  
Vol 35 (2) ◽  
pp. 186-193 ◽  
Author(s):  
Tamayo Murase ◽  
Takuya Hattori ◽  
Masafumi Ohtake ◽  
Mayuna Abe ◽  
Yui Amakusa ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Animal Model ◽  
Diastolic Dysfunction ◽  
Cardiac Remodeling

Exercise training protects against cancer-induced cardiac remodeling in an animal model of urothelial carcinoma

2018 ◽  
Vol 645 ◽  
pp. 12-18 ◽  
Author(s):  
Ana Isabel Padrão ◽  
Rita Nogueira-Ferreira ◽  
Rui Vitorino ◽  
Dulce Carvalho ◽  
Catarina Correia ◽  
...  
Keyword(s):  
Animal Model ◽  
Exercise Training ◽  
Urothelial Carcinoma ◽  
Cardiac Remodeling

Cardiac remodeling after reduction of high-flow arteriovenous fistulas in end-stage renal disease

2016 ◽  
Vol 39 (9) ◽  
pp. 654-659 ◽  
Author(s):  
Peter Wohlfahrt ◽  
Slavomir Rokosny ◽  
Vojtech Melenovsky ◽  
Barry A Borlaug ◽  
Vera Pecenkova ◽  
...  
Keyword(s):  
Renal Disease ◽  
Cardiac Remodeling ◽  
End Stage Renal Disease ◽  
High Flow ◽  
Arteriovenous Fistulas ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Up-regulating autophagy by targeting the mTOR-4EBP1 pathway: a possible mechanism for improving cardiac function in mice with experimental dilated cardiomyopathy

2020 ◽  
Author(s):  
Bo Jin ◽  
Haiming Shi ◽  
Zhu Jun ◽  
Bangwei Wu ◽  
Quzhen Geshang
Keyword(s):  
Animal Model ◽  
Cardiovascular Diseases ◽  
Cardiac Function ◽  
Dilated Cardiomyopathy ◽  
Cardiac Remodeling ◽  
Therapeutic Strategy ◽  
Volume Fraction ◽  
Pathological Process ◽  
Cardiac Myosin ◽  
Pathological Mechanism

Abstract Background: Autophagy plays a crucial role in the pathological process of cardiovascular diseases. However, little is known about the pathological mechanism underlying autophagy regulation in dilated cardiomyopathy (DCM). Methods: We explored whether up-regulating autophagy could improve cardiac function in mice with experimental DCM through the mTOR-4EBP1 pathway. Animal model of DCM was established in BALB/c mice by immunization with porcine cardiac myosin. Both up- or down-regulation of autophagy were studied by administration of rapamycin or 3-MA in parallel. Morphology, Western blotting, and echocardiography were applied to confirm the pathological mechanisms. Results: Autophagy was activated and autophagosomes were significantly increased in the rapamycin group. The collagen volume fraction (CVF) was decreased in the rapamycin group compared with the DCM group (9.21 ± 0.82 % vs 14.38 ± 1.24 %, P<0.01). The expression of p-mTOR and p-4EBP1 were significantly decreased in rapamycin-induced autophagy activation, while the levels were increased by down-regulating autophagy with 3-MA. In the rapamycin group, the LVEF and FS were significantly increased compared with the DCM group (54.12 ± 6.48 % vs 45.29 ± 6.68 %, P <0.01; 26.89 ± 4.04 % vs 22.17 ± 2.82 %, P <0.05). As the inhibitor of autophagy, 3-MA aggravated the progress of maladaptive cardiac remodeling and declined cardiac function in DCM mice. Conclusions: The study indicated a possible mechanism for improving cardiac function in mice with experimental DCM by up-regulating autophagy via the mTOR-4EBP1 pathway, which could be a promising therapeutic strategy for DCM.

scholarly journals Up-regulating autophagy by targeting the mTOR-4EBP1 pathway: a possible mechanism for improving cardiac function in mice with experimental dilated cardiomyopathy

2019 ◽  
Author(s):  
Bo Jin ◽  
Haiming Shi ◽  
Zhu Jun ◽  
Bangwei Wu ◽  
Quzhen Geshang
Keyword(s):  
Animal Model ◽  
Cardiovascular Diseases ◽  
Cardiac Function ◽  
Dilated Cardiomyopathy ◽  
Cardiac Remodeling ◽  
Therapeutic Strategy ◽  
Volume Fraction ◽  
Pathological Process ◽  
Cardiac Myosin ◽  
Pathological Mechanism

Abstract Background: Autophagy plays a crucial role in the pathological process of cardiovascular diseases. However, little is known about the pathological mechanism underlying autophagy regulation in dilated cardiomyopathy (DCM).Methods: We explored whether up-regulating autophagy could improve cardiac function in mice with experimental DCM through the mTOR-4EBP1 pathway. Animal model of DCM was established in BALB/c mice by immunization with porcine cardiac myosin. Both up- or down-regulation of autophagy were studied by administration of rapamycin or 3-MA in parallel. Morphology, Western blotting, and echocardiography were applied to confirm the pathological mechanisms.Results: Autophagy was activated and autophagosomes were significantly increased in the rapamycin group. The collagen volume fraction (CVF) was decreased in the rapamycin group compared with the DCM group (9.21 ± 0.82 % vs 14.38 ± 1.24 %, P<0.01). The expression of p-mTOR and p-4EBP1 were significantly decreased in rapamycin-induced autophagy activation, while the levels were increased by down-regulating autophagy with 3-MA. In the rapamycin group, the LVEF and FS were significantly increased compared with the DCM group (54.12 ± 6.48 % vs 45.29 ± 6.68 %, P<0.01; 26.89 ± 4.04 % vs 22.17 ± 2.82 %, P<0.05). As the inhibitor of autophagy, 3-MA aggravated the progress of maladaptive cardiac remodeling and declined cardiac function in DCM mice.Conclusions: The study indicated a possible mechanism for improving cardiac function in mice with experimental DCM by up-regulating autophagy via the mTOR-4EBP1 pathway, which could be a promising therapeutic strategy for DCM.

Exposure to Hydrocarbons and Renal Disease: An Experimental Animal Model

Renal Failure ◽  
1999 ◽  
Vol 21 (3-4) ◽  
pp. 369-385 ◽  
Author(s):  
A. Mutti ◽  
T. Coccini ◽  
R. Alinovi ◽  
G. Toubeau ◽  
F. Broeckaert ◽  
...  
Keyword(s):  
Animal Model ◽  
Renal Disease ◽  
Experimental Animal ◽  
Experimental Animal Model

scholarly journals Up-regulating autophagy by targeting the mTOR-4EBP1 pathway: a possible mechanism for improving cardiac function in mice with experimental dilated cardiomyopathy

2020 ◽  
Author(s):  
Bo Jin ◽  
Haiming Shi ◽  
Zhu Jun ◽  
Bangwei Wu ◽  
Quzhen Geshang
Keyword(s):  
Animal Model ◽  
Cardiovascular Diseases ◽  
Cardiac Function ◽  
Dilated Cardiomyopathy ◽  
Cardiac Remodeling ◽  
Therapeutic Strategy ◽  
Volume Fraction ◽  
Pathological Process ◽  
Cardiac Myosin ◽  
Pathological Mechanism

Abstract Background: Autophagy plays a crucial role in the pathological process of cardiovascular diseases. However, little is known about the pathological mechanism underlying autophagy regulation in dilated cardiomyopathy (DCM).Methods: We explored whether up-regulating autophagy could improve cardiac function in mice with experimental DCM through the mTOR-4EBP1 pathway. Animal model of DCM was established in BALB/c mice by immunization with porcine cardiac myosin. Both up- or down-regulation of autophagy were studied by administration of rapamycin or 3-MA in parallel. Morphology, Western blotting, and echocardiography were applied to confirm the pathological mechanisms.Results: Autophagy was activated and autophagosomes were significantly increased in the rapamycin group. The collagen volume fraction (CVF) was decreased in the rapamycin group compared with the DCM group (9.21 ± 0.82 % vs 14.38 ± 1.24 %, P<0.01). The expression of p-mTOR and p-4EBP1 were significantly decreased in rapamycin-induced autophagy activation, while the levels were increased by down-regulating autophagy with 3-MA. In the rapamycin group, the LVEF and FS were significantly increased compared with the DCM group (54.12 ± 6.48 % vs 45.29 ± 6.68 %, P<0.01; 26.89 ± 4.04 % vs 22.17 ± 2.82 %, P<0.05). As the inhibitor of autophagy, 3-MA aggravated the progress of maladaptive cardiac remodeling and declined cardiac function in DCM mice.Conclusions: The study indicated a possible mechanism for improving cardiac function in mice with experimental DCM by up-regulating autophagy via the mTOR-4EBP1 pathway, which could be a promising therapeutic strategy for DCM.

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