Multifunctional protein: cardiac ankyrin repeat protein

Zhang, Na; Xie, Xing; Wang, Jianan

doi:10.1631/jzus.b1500247

Cited by 12 publications

(16 citation statements)

References 64 publications

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“…Consequently, sarcomere disarray and loss of myofilaments leads to abnormal cardiac contractility. 69,70 It is suggested that GATA-4 and CARP co-dependency is needed for sarcomere organization and functioning, while dox overts their association during myofibrillar disarray and hypertrophy. 71 Combining the above stated facts, it can be understood that DOX interrupts cardiac contractile and pumping machinery through sarcomeric genes such as actin, TnI, MLC2, and CK-M, without affecting skeletal myocytes.…”

Section: Dox and The Cardiac Sarcomere Proteinsmentioning

confidence: 99%

“…It is observed that the level and activity of CARP is suppressed by DOX, which is connected to dilated and hypertrophic cardiomyopathy and skeletal muscle myopathies. Consequently, sarcomere disarray and loss of myofilaments leads to abnormal cardiac contractility 69,70 . It is suggested that GATA‐4 and CARP co‐dependency is needed for sarcomere organization and functioning, while dox overts their association during myofibrillar disarray and hypertrophy 71 …”

Section: Effects Of Dox On the Cardiac Regimementioning

confidence: 99%

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A short review: Doxorubicin and its effect on cardiac proteins

Upadhyay

Gupta

Mantha

et al. 2020

J of Cellular Biochemistry

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Doxorubicin (DOX) is a boon for cancer‐suffering patients. However, the undesirable effect on health on vital organs, especially the heart, is a limiting factor, resulting in an increased number of patients with cardiac dysfunction. The present review focuses on the contractile machinery and associated factors, which get affected due to DOX toxicity in chemo‐patients for which they are kept under life‐long investigation for cardiac function. DOX‐induced oxidative stress disrupts the integrity of cardiac contractile muscle proteins that alter the rhythmic mechanism and oxygen consumption rate of the heart. DOX is an oxidant and it is further discussed that oxidative stress prompts the damage of contractile components and associated factors, which include Ca2+ load through Ca2+ ATPase, SERCA, ryanodine receptor‐2, phospholamban, and calsequestrin, which ultimately results in left ventricular ejection and dilation. Based on data and evidence, the associated proteins can be considered as clinical markers to develop medications for patients. Even with the advancement of various diagnosing tools and modified drugs to mitigate DOX‐induced cardiotoxicity, the risk could not be surmounted with survivors of cancer.

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Section: Dox and The Cardiac Sarcomere Proteinsmentioning

confidence: 99%

Section: Effects Of Dox On the Cardiac Regimementioning

confidence: 99%

A short review: Doxorubicin and its effect on cardiac proteins

Upadhyay

Gupta

Mantha

et al. 2020

J of Cellular Biochemistry

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“…Representative genes from the top 6 most significantly differentially regulated signaling pathways activated by SV serum-treatment including ceramide, p38 MAPK, PLC, cardiac hypertrophy, actin cytoskeleton, and oxidative stress response signaling (Figure S2) were chosen for further analysis. Confirmatory analysis by RT-qPCR was performed on human RV tissue for representative genes in each pathway, including (1) ceramide kinase CERK 31 , (2) cyclic AMP-responsive transcription factor CREB5 32,33 , (3) non-receptor tyrosine kinase FYN 34,35 , (4) cardiac ankyrin repeat domain ANKRD1 36,37 , (5) α-actinin isoform ACTN2 38,39 , and (6) transcription factor MAFK 40 . RT-qPCR revealed that these representative genes were significantly upregulated in SV RV relative to NF control RV, consistent with the SV-sera NRVM treatment findings (Figure 8).…”

Section: Resultsmentioning

confidence: 99%

Phosphodiesterase-5 Is Elevated in Failing Single Ventricle Myocardium and Affects Cardiomyocyte Remodeling In Vitro

Garcia

Karimpour-Fard²,

Nunley³

et al. 2018

Circ: Heart Failure

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Background: Single ventricle congenital heart disease (SV) is fatal without intervention and eventual heart failure (HF) is a major cause of morbidity and mortality. While there are no proven medical therapies for the treatment or prevention of HF in the SV population, phosphodiesterase-5 inhibitors (PDE5i), such as sildenafil, are increasingly utilized. While the pulmonary vasculature is the primary target of PDE5i therapy in patients with SV, the effects of PDE5i on the SV myocardium remain largely unknown. We sought to determine PDE5 expression and activity in the single right ventricle (RV) of SV patients relative to non-failing (NF) controls, and to determine if PDE5 impacts cardiomyocyte remodeling using a novel serum based in vitro model. Methods and Results: PDE5 expression (n=9 NF, n=7 SV), activity (n=8 NF, n=9 SV) and localization (n=3 SV) were determined in explanted human RV myocardium. PDE5 is expressed in SV cardiomyocytes and PDE5 protein expression and activity are increased in SV RV compared to NF RV. Isolated neonatal rat ventricular myocytes (NRVMs) were treated for 72 hours with NF or SV patient serum ± sildenafil. RT-qPCR (n=5 NF, n=12 SV) and RNAseq (n=3 NF, n=3 SV) were performed on serum-treated NRVMs and demonstrated that treatment with SV sera results in pathological gene expression changes which are attenuated with PDE5i. Conclusions: PDE5 is increased in failing SV myocardium and pathologic gene expression changes in SV serum-treated NRVMs are abrogated by PDE5i. These results suggest that PDE5 represents an intriguing myocardial therapeutic target in this population.

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“…[ 18 ] Moreover, its interference on the iron metabolism (Fe 3+ ) [ 34 ] and in the cardiac synthesis of ankyrin repeat protein increases reactive oxygen species production and compromises the myocyte survival and cellular transcription, respectively. [ 35 ] In a prospective study, an increase in proapoptotic proteins (sFas and sTRAIL) was detected 1 year after the end of the chemotherapy treatment for breast cancer, evidencing the chronic residual effects of this treatment. [ 36 ] However, the authors did not find a correlation between these biomarkers levels with the predictive risk of cardiac dysfunction or with the subclinical alterations in the left ventricle ejection fraction and NT-proBNP levels (a biomarker of heart failure), also detected in the study.…”

Section: Discussionmentioning

confidence: 99%

Effects of treatment with chemotherapy and/or tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer

Silva¹,

Romero

Carvalho³

et al. 2017

Medicine

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There has been an increase in deaths from cardiovascular diseases following breast cancer therapy. Evidence has shown that this outcome is, in part, associated with cardiotoxicity induced by the chemotherapeutic drugs and the increase in oxidative stress. The aim of this study was to evaluate the effects of chemotherapy and hormone therapy with tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer.Thirty women were followed-up for 1 year and were divided into 3 groups according to the treatment protocol: women treated only with tamoxifen and clinical follow up for 12 months (Tam, n = 10); women treated only with chemotherapy for 6 months with clinical follow up for an additional 6-month period (Chemo, n = 10); and women who received chemotherapy for 6 months followed by a 6-month period only with tamoxifen therapy and clinical follow up (Chemo + Tam, n = 10). Analysis of the blood levels of cardiac troponin I (cTnI), advanced oxidation protein products (AOPP) and the activity of the plasmatic isoform of the antioxidant enzyme glutathione peroxidase (GPx) was performed before treatment (T0) and at 6 (T6) and 12 (T12) months after treatment.The Chemo group showed higher levels of cTnI (0.065 ± 0.006 ng/mL, P < .05) and AOPP (4.99 ± 0.84 μmol/L, P < .05) and reduced GPx activity (24.4 ± 1.1 nM/min/mL, P < .05) at T12 than the Tam group (cTnI: 0.031 ± 0.001 ng/mL; AOPP: 1.40 ± 0.10 μmol/L; GPx: 28.0 ± 0.7 nM/min/mL) and Chemo + Tam group (cTnI: 0.037 ± 0.002 ng/mL; AOPP: 2.53 ± 0.30 μmol/L; GPx: 29.5 ± 1.0 nM/min/mL).These data support the hypothesis that long-term oxidative stress after chemotherapy may have an impact on cardiovascular diseases and that tamoxifen has cardioprotective effects.

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Multifunctional protein: cardiac ankyrin repeat protein

Cited by 12 publications

References 64 publications

A short review: Doxorubicin and its effect on cardiac proteins

A short review: Doxorubicin and its effect on cardiac proteins

Phosphodiesterase-5 Is Elevated in Failing Single Ventricle Myocardium and Affects Cardiomyocyte Remodeling In Vitro

Effects of treatment with chemotherapy and/or tamoxifen on the biomarkers of cardiac injury and oxidative stress in women with breast cancer

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