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Oxymatrine alleviates ALD-induced cardiac hypertrophy by regulating autophagy via activation Nrf2/SIRT3 signaling pathway.

Phytomedicine

January 2025

The State Key Laboratory of Functions and Applications of Medicinal Plants (The Key Laboratory of Endemic and Ethnic Diseases of Ministry of Education), Guizhou Medical University, No.6 Ankang Avenue, Guiyang City and Guian New District, Guizhou 561113, China; The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province (The high educational key laboratory of Guizhou province for natural medicianl Pharmacology and Druggability), Guizhou Medical University, No.6 Ankang Avenue, Guiyang City and Guian New District, Guizhou 561113, China; The Department of Pharmacology of Materia Medica, School of Pharmaceutical Sciences, Guizhou Medical University, No.6 Ankang Avenue, Guiyang City and Guian New District, Guizhou 561113, China. Electronic address:

Background: Cardiac hypertrophy is a prevalent early pathological manifestation in various cardiovascular diseases, lacking effective interventions to impede its progression. Although oxymatrine (OMT) has shown potential benefits for cardiac function, its therapeutic efficacy and mechanism in cardiac hypertrophy remain incompletely understood. Notably, mitochondrial damage and dysregulated autophagy are pivotal pathogenic mechanisms in cardiac hypertrophy.

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Background: Cardiac fibrosis plays a critical role in the progression of various forms of heart disease, significantly increasing the risk of sudden cardiac death. However, currently, there are no therapeutic strategies available to prevent the onset of cardiac fibrosis.

Methods And Results: Here, biomimetic ATP-responsive nanozymes based on genetically engineered cell membranes are adapted to specifically recognize activated cardiac fibroblasts (CFs) for the treatment of cardiac fibrosis.

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The maintenance of intracellular and extracellular adenosine triphosphate (ATP) levels plays a pivotal role in cardiac function. In recent years, burgeoning attention has been directed towards ATP-induced cell death (AICD), revealing it as a distinct cellular demise pathway triggered by heightened extracellular ATP concentrations, distinguishing it from other forms of cell death such as apoptosis and necrosis. AICD is increasingly acknowledged as a critical mechanism mediating the pathogenesis and progression of various cardiovascular maladies, encompassing myocardial ischemia-reperfusion injury, sepsis-induced cardiomyopathy, hypertrophic cardiomyopathy, arrhythmia, and diabetic cardiomyopathy.

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Objectives: The development and progression of chronic heart failure (CHF), hypertrophy, and remodeling strongly correlate with myocardial inflammation and oxidative stress. S-adenosylmethionine (SAMe), available as a dietary supplement, exerts anti-inflammatory and antioxidant effects. Previous reports show that by regulating angiogenesis and fibrosis, S-adenosyl-L-methionine improves ventricular remodeling.

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Importance: Long-term use of anabolic androgenic steroids (AASs) is associated with a high risk of left ventricular hypertrophy, heart failure with reduced systolic function, and early sudden death, with the mechanism of progression being understudied. Early and persistent impaired myocardial microcirculation could be of clinical importance and a potential underlying mechanism of frequent and early cardiac disease among individuals with AAS use and a future potential target for intervention.

Objective: To investigate coronary microcirculation by measuring myocardial flow reserve (MFR) in men with current and former AAS use compared with controls with no prior AAS use, using cardiac rubidium 82 (82Rb) positron emission tomography/computed tomography (PET/CT).

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