Cardiomyocyte Specific Deletion of ADAR1 Causes Severe Cardiac Dysfunction and Increased Lethality

Cardiac-specific Deletion of SOCS3 Improved Lipopolysaccharide-Induced Cardiac Dysfunction via Mitochondria Stabilization

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2009.07.157 ◽

2009 ◽

Vol 15 (7) ◽

pp. S183

Author(s):

Nobuyoshi Futamata ◽

Hideo Yasukawa ◽

Toyoharu Oba ◽

Kazutoshi Mawatari ◽

Takanobu Nagata ◽

...

Keyword(s):

Cardiac Dysfunction ◽

Specific Deletion

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Heart Specific Deletion of RNA Binding Protein Rbfox1 Sensitizes Mice to Pressure Overload Induced Cardiac Dysfunction

The FASEB Journal ◽

10.1096/fasebj.29.1_supplement.553.2 ◽

2015 ◽

Vol 29 (S1) ◽

Author(s):

Wuqiang Zhu ◽

Ingrid Bender ◽

Amritha Yellamilli ◽

Jop Berlo

Keyword(s):

Cardiac Dysfunction ◽

Rna Binding ◽

Binding Protein ◽

Rna Binding Protein ◽

Pressure Overload ◽

Specific Deletion

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Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model

International Journal of Cardiology ◽

10.1016/j.ijcard.2018.01.013 ◽

2018 ◽

Vol 259 ◽

pp. 145-152 ◽

Cited By ~ 6

Author(s):

Manisha Gupte ◽

Samvruta Tumuluru ◽

Jennifer Y. Sui ◽

Anand Prakash Singh ◽

Prachi Umbarkar ◽

...

Keyword(s):

Cardiac Dysfunction ◽

Diet Induced Obesity ◽

Gsk 3Β ◽

Specific Deletion

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SIRT1 Activation Attenuates the Cardiac Dysfunction Induced by Endothelial Cell-Specific Deletion of CRIF1

Biomedicines ◽

10.3390/biomedicines9010052 ◽

2021 ◽

Vol 9 (1) ◽

pp. 52

Author(s):

Shuyu Piao ◽

Ikjun Lee ◽

Seon-Ah Jin ◽

Seonhee Kim ◽

Harsha Nagar ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cell ◽

Cardiac Function ◽

Cardiac Dysfunction ◽

Mitochondrial Protein ◽

Weight Ratio ◽

Sirtuin 1 ◽

Endothelial Junction ◽

Endothelial Nitric Oxide ◽

Specific Deletion

The CR6-interacting factor1 (CRIF1) mitochondrial protein is indispensable for peptide synthesis and oxidative phosphorylation. Cardiomyocyte-specific deletion of CRIF1 showed impaired mitochondrial function and cardiomyopathy. We developed an endothelial cell-specific CRIF1 deletion mouse to ascertain whether dysfunctional endothelial CRIF1 influences cardiac function and is mediated by the antioxidant protein sirtuin 1 (SIRT1). We also examined the effect of the potent SIRT1 activator SRT1720 on cardiac dysfunction. Mice with endothelial cell-specific CRIF1 deletion showed an increased heart-to-body weight ratio, increased lethality, and markedly reduced fractional shortening of the left ventricle, resulting in severe cardiac dysfunction. Moreover, endothelial cell-specific CRIF1 deletion resulted in mitochondrial dysfunction, reduced ATP levels, inflammation, and excessive oxidative stress in heart tissues, associated with decreased SIRT1 expression. Intraperitoneal injection of SRT1720 ameliorated cardiac dysfunction by activating endothelial nitric oxide synthase, reducing oxidative stress, and inhibiting inflammation. Furthermore, the decreased endothelial junction-associated protein zonula occludens-1 in CRIF1-deleted mice was significantly recovered after SRT1720 treatment. Our results suggest that endothelial CRIF1 plays an important role in maintaining cardiac function, and that SIRT1 induction could be a therapeutic strategy for endothelial dysfunction-induced cardiac dysfunction.

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High Dietary Phosphate Exacerbates and Acts Independently of Low Autophagy Activity in Pathological Cardiac Remodeling and Dysfunction

Cells ◽

10.3390/cells10040777 ◽

2021 ◽

Vol 10 (4) ◽

pp. 777

Author(s):

Mingjun Shi ◽

Sierra Shepard ◽

Zhiyong Zhou ◽

Jenny Maique ◽

Olivia Seli ◽

...

Keyword(s):

Cardiac Remodeling ◽

Cardiac Dysfunction ◽

Related Protein ◽

Short Lifespan ◽

Uremic Cardiomyopathy ◽

Dietary Phosphate ◽

Lc3 Puncta ◽

Autophagy Activity ◽

Specific Deletion ◽

High Phosphate

High phosphate contributes to uremic cardiomyopathy. Abnormal autophagy is associated with the development and progression of heart disease. What is unknown is the effects of phosphate on autophagy and whether the ill effects of phosphate on cardiomyocytes are mediated by low autophagy. High (2.0% w/w)-phosphate diet reduced LC3 puncta in cardiomyocytes and ratio of LC3 II/I and increased p62 protein, indicating that autophagy activity was suppressed. Mice with cardiomyocyte-specific deletion of autophagy-related protein 5 (H-atg5−/−) had reduced autophagy only in the heart, developed cardiac dysfunction with hypertrophy and fibrosis, and had a short lifespan. When H-atg5−/− mice were fed a high-phosphate diet, they developed more apoptosis in cardiomyocytes, more severe cardiac remodeling, and shorter lifespan than normal phosphate-fed H-atg5−/− mice, indicating that cardiac phosphotoxicity is imparted independently of atg5. In conclusion, although high phosphate suppresses autophagy, high phosphate and low autophagy independently trigger and additionally amplify cardiac remodeling and dysfunction.

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