scholarly journals Regulation of Sirtuin-Mediated Protein Deacetylation by Cardioprotective Phytochemicals

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Niria Treviño-Saldaña ◽  
Gerardo García-Rivas
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Posttranslational Modifications ◽  
Cardiac Dysfunction ◽  
Therapeutic Strategy ◽  
Alpha Lipoic Acid ◽  
Protein Acetylation ◽  
Cardioprotective Effects ◽  
Expression And Activity ◽  
Novel Therapeutic

Modulation of posttranslational modifications (PTMs), such as protein acetylation, is considered a novel therapeutic strategy to combat the development and progression of cardiovascular diseases. Protein hyperacetylation is associated with the development of numerous cardiovascular diseases, including atherosclerosis, hypertension, cardiac hypertrophy, and heart failure. In addition, decreased expression and activity of the deacetylases Sirt1, Sirt3, and Sirt6 have been linked to the development and progression of cardiac dysfunction. Several phytochemicals exert cardioprotective effects by regulating protein acetylation levels. These effects are mainly exerted via activation of Sirt1 and Sirt3 and inhibition of acetyltransferases. Numerous studies support a cardioprotective role for sirtuin activators (e.g., resveratrol), as well as other emerging modulators of protein acetylation, including curcumin, honokiol, oroxilyn A, quercetin, epigallocatechin-3-gallate, bakuchiol, tyrosol, and berberine. Studies also point to a cardioprotective role for various nonaromatic molecules, such as docosahexaenoic acid, alpha-lipoic acid, sulforaphane, and caffeic acid ethanolamide. Here, we review the vast evidence from the bench to the clinical setting for the potential cardioprotective roles of various phytochemicals in the modulation of sirtuin-mediated deacetylation.

Subcutaneous BNP administration in experimental mild heart failure: A novel therapeutic strategy

1998 ◽  
Vol 4 (3) ◽  
pp. 19
Author(s):  
HH Chen ◽  
JA Grantham ◽  
JA Schirger ◽  
M Jougasaki ◽  
O Lisy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Therapeutic Strategy ◽  
Mild Heart Failure ◽  
Novel Therapeutic

scholarly journals FKBP12.6-Mediated Stabilization of Calcium-Release Channel (Ryanodine Receptor) as a Novel Therapeutic Strategy Against Heart Failure

Circulation ◽  
2003 ◽  
Vol 107 (3) ◽  
pp. 477-484 ◽  
Author(s):  
Masafumi Yano ◽  
Shigeki Kobayashi ◽  
Masateru Kohno ◽  
Masahiro Doi ◽  
Takahiro Tokuhisa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ryanodine Receptor ◽  
Therapeutic Strategy ◽  
Calcium Release ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Novel Therapeutic

scholarly journals The Effects of Guizhi Gancao Decoction on Pressure Overload-Induced Heart Failure and Posttranslational Modifications of Tubulin in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Hui-hua Chen ◽  
Pei Zhao ◽  
Jing Tian ◽  
Wei Guo ◽  
Ming Xu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Posttranslational Modifications ◽  
Volume Fraction ◽  
Pressure Overload ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Immunofluorescent Analysis ◽  
Traditional Chinese Medical ◽  
Hemodynamic Measurements

Guizhi Gancao Decoction (GGD), a traditional Chinese medical recipe, has been widely used in the treatment of cardiovascular diseases in China for centuries. The present study was carried out to determine whether GGD exerts direct protective effects against pressure overload-induced heart failure. Moreover, we investigated whether GGD affects tubulin expression and posttranslational modifications. We demonstrated that GGD ameliorated TAC caused cardiac hypertrophy by gravimetric and echocardiography analysis in C57BL/6 mice. We found that GGD abrogated TAC-induced myocardium fibrosis by Masson’s staining and collagen volume fraction (CVF) analysis. By using pressure-volume hemodynamic measurements, we found that GGD prevented TAC-induced cardiac systolic and diastolic dysfunction. Immunoblotting and immunofluorescent analysis revealed that GGD abrogated TAC-induced detyrosination and acetylation abnormalities on microtubules. Our present study demonstrated potential therapeutic effects of GGD against pressure overload-induced heart failure.

DNA methylation inhibition: A novel therapeutic strategy for heart failure

2014 ◽  
Vol 176 (1) ◽  
pp. 232-233 ◽  
Author(s):  
Yu-Hsun Kao ◽  
Gi-Shih Lien ◽  
Tze-Fan Chao ◽  
Yi-Jen Chen
Keyword(s):  
Heart Failure ◽  
Dna Methylation ◽  
Therapeutic Strategy ◽  
Novel Therapeutic

scholarly journals Blockade of NKG2D / NKG2D ligands interaction as a novel therapeutic strategy against heart failure

2018 ◽  
Vol WCP2018 (0) ◽  
pp. OR2-3
Author(s):  
Kotaro Matsumoto ◽  
Masanori Obana ◽  
Makiko Maeda ◽  
Hiroyuki Nakayama ◽  
Yasushi Fujio
Keyword(s):  
Heart Failure ◽  
Therapeutic Strategy ◽  
Nkg2d Ligands ◽  
Novel Therapeutic

scholarly journals CaMKII Inhibition is a Novel Therapeutic Strategy to Prevent Diabetic Cardiomyopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Christopher R. Veitch ◽  
Amelia S. Power ◽  
Jeffrey R. Erickson
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Therapeutic Strategy ◽  
Complex Disease ◽  
Positive Impact ◽  
Critical Examination ◽  
Diabetic Patients ◽  
Protective Effects ◽  
Camkii Activation ◽  
Novel Therapeutic

Increasing prevalence of diabetes mellitus worldwide has pushed the complex disease state to the foreground of biomedical research, especially concerning its multifaceted impacts on the cardiovascular system. Current therapies for diabetic cardiomyopathy have had a positive impact, but with diabetic patients still suffering from a significantly greater burden of cardiac pathology compared to the general population, the need for novel therapeutic approaches is great. A new therapeutic target, calcium/calmodulin-dependent kinase II (CaMKII), has emerged as a potential treatment option for preventing cardiac dysfunction in the setting of diabetes. Within the last 10 years, new evidence has emerged describing the pathophysiological consequences of CaMKII activation in the diabetic heart, the mechanisms that underlie persistent CaMKII activation, and the protective effects of CaMKII inhibition to prevent diabetic cardiomyopathy. This review will examine recent evidence tying cardiac dysfunction in diabetes to CaMKII activation. It will then discuss the current understanding of the mechanisms by which CaMKII activity is enhanced during diabetes. Finally, it will examine the benefits of CaMKII inhibition to treat diabetic cardiomyopathy, including contractile dysfunction, heart failure with preserved ejection fraction, and arrhythmogenesis. We intend this review to serve as a critical examination of CaMKII inhibition as a therapeutic strategy, including potential drawbacks of this approach.

scholarly journals EDITORIAL: THORACIC DUCT DECOMPRESSION: AN IDEA WHOSE TIME HAS COME – AGAIN

Lymphology ◽  
2020 ◽  
Vol 53 (2) ◽  
Author(s):  
MH Witte
Keyword(s):  
Heart Failure ◽  
Portal Hypertension ◽  
Thoracic Duct ◽  
Therapeutic Strategy ◽  
Hepatic Cirrhosis ◽  
Venous Hypertension ◽  
Central Venous ◽  
Image Guided ◽  
Central Venous Hypertension ◽  
Novel Therapeutic

Thoracic duct decompression (TDD) is an idea first proposed and applied as a novel therapeutic strategy by lymphologists in the 1960's. TDD is recently being reexamined and, in selected patients with portal hypertension from hepatic cirrhosis or with central venous hypertension from isolated right-sided heart failure, undertaken using advanced surgical and image-guided interventional radiologic approaches.

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