Documenting the Global Burden of Cardiovascular Disease

Yusuf, Salim

doi:10.1161/circulationaha.114.008302

Cited by 17 publications

(9 citation statements)

References 29 publications

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“…Cardiovascular diseases (CVDs) are the leading cause of death among non-communicable diseases [1]. The hallmarks of CVD include cardiac hypertrophy and increased incidence of cardiovascular events, such as ischemic episode, arrhythmias, and sudden death [2,3].…”

Section: Introductionmentioning

confidence: 99%

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Gitau

Zhao

et al. 2015

Front. Med.

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Ventricular hypertrophy is a powerful and independent predictor of cardiovascular morbid events. The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail. In this study, healthy wild-type male mice were randomly divided into three groups and subjected to transverse aortic constriction (TAC) or sham operation. The TAC-operated mice were treated with the human equivalent of low-dose aspirin (10 mg$kg); the remaining mice received an equal amount of phosphate buffered saline with 0.65% ethanol, which was used as a vehicle. A cardiomyocyte hypertrophy model induced by angiotensin II (10 nmol$L -1 ) was treated with the human equivalent of low (10 or 100 µmol$L ) aspirin concentrations in plasma. Changes in the cardiac structure and function were assessed through echocardiography and transmission electron microscopy. Gene expression was determined through RT-PCR and western blot analysis. Results indicated that aspirin treatment abrogated the increased thickness of the left ventricular anterior and posterior walls, the swelling of mitochondria, and the increased surface area in in vivo and in vitro hypertrophy models. Aspirin also normalized the upregulated hypertrophic biomarkers, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP). Aspirin efficiently reversed the upregulation of β-catenin and P-Akt expression and the TAC-or ANG II-induced downregulation of GSK-3β. Therefore, low-dose aspirin possesses significant anti-hypertrophic properties at clinically relevant concentrations for anti-thrombotic therapy. The downregulation of β-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.

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Section: Introductionmentioning

confidence: 99%

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Gitau

Zhao

et al. 2015

Front. Med.

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“…Acute myocardial infarction (AMI), or heart attack, is one of the leading causes of death throughout the world and is responsible for the occurrence of critical life-threatening conditions. The clinical confirmation of AMI and heart failure is performed through the detection of cardiovascular biomarkers such as cardiac troponin I (cTnI), B-type natriuretic peptide (BNP), and myoglobin (Myo) [ 38 ]. Ji et al presented a biosensor composed of porous hydrogel-encapsulated photonic crystals (PhCs) to detect and quantify these biomarker proteins [ 39 ].…”

Section: Biomedical Applicationsmentioning

confidence: 99%

Hydrogel-Based Biosensors

Völlmecke

Afroz

Bierbach

et al. 2022

Gels

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There is an increasing interest in sensing applications for a variety of analytes in aqueous environments, as conventional methods do not work reliably under humid conditions or they require complex equipment with experienced operators. Hydrogel sensors are easy to fabricate, are incredibly sensitive, and have broad dynamic ranges. Experiments on their robustness, reliability, and reusability have indicated the possible long-term applications of these systems in a variety of fields, including disease diagnosis, detection of pharmaceuticals, and in environmental testing. It is possible to produce hydrogels, which, upon sensing a specific analyte, can adsorb it onto their 3D-structure and can therefore be used to remove them from a given environment. High specificity can be obtained by using molecularly imprinted polymers. Typical detection principles involve optical methods including fluorescence and chemiluminescence, and volume changes in colloidal photonic crystals, as well as electrochemical methods. Here, we explore the current research utilizing hydrogel-based sensors in three main areas: (1) biomedical applications, (2) for detecting and quantifying pharmaceuticals of interest, and (3) detecting and quantifying environmental contaminants in aqueous environments.

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“…With the population growth and aging, the global burden of ischemic heart disease (IHD) is high [ 1 , 2 ]. How to repair traumatic myocardium, reverse ventricle remodeling, and improve heart function after myocardial infarction (MI) are the main problems facing clinicians.…”

Section: Introductionmentioning

confidence: 99%

Blockade of RBP-J-Mediated Notch Signaling Pathway Exacerbates Cardiac Remodeling after Infarction by Increasing Apoptosis in Mice

Pang

Huang

et al. 2018

BioMed Research International

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Background Ischemic heart disease (IHD) is the major cause of death in patients with cardiovascular disease. Cardiac remodeling is a common pathological change following myocardial infarction (MI), and cardiomyocyte apoptosis plays a key role in this change. Transcription factor recombination signal-binding protein-J (RBP-J)-mediated Notch signaling pathway has been implicated in several inherited cardiovascular diseases, including aortic valve diseases, but whether the RBP-J-mediated Notch signaling pathway plays a role in cardiomyocyte apoptosis after MI is unclear. Method We crossed RBP-Jfl/fl mice and Myh6-Cre/Esr1 transgenic mice to delete RBP-J in vivo and to partly inhibit the canonical Notch signaling pathway. MI was induced in mice by permanent ligation of the left anterior descending coronary artery followed by the knockout of RBP-J. Cardiac function and morphology were assessed by echocardiography and histological analysis 4 weeks after infarction. In addition, the expression and regulation of apoptosis-related molecules were examined by real time PCR and western blot. Results RBP-J knockout decreased the survival rate and deteriorated post-MI remodeling and function in mice, and this effect was associated with increased cardiomyocyte apoptosis. The potential mechanisms might be related to the downregulated expression of bcl-2, upregulated expression of bax, and cleaved-caspase 3 to exacerbate cardiomyocyte apoptosis. Conclusion These findings show that the RBP-J-mediated Notch signaling pathway in cardiomyocytes limits ventricular remodeling and improves cardiac function after MI. The RBP-J-mediated Notch signaling pathway has a protective role in cardiomyocyte apoptosis following cardiac injury.

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Documenting the Global Burden of Cardiovascular Disease

Cited by 17 publications

References 29 publications

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling

Hydrogel-Based Biosensors

Blockade of RBP-J-Mediated Notch Signaling Pathway Exacerbates Cardiac Remodeling after Infarction by Increasing Apoptosis in Mice

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