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

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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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Irbesartan improves ventricular remodeling (VR) following myocardial infarction (MI). This study investigates whether irbesartan attenuates VR by reducing aldosterone production in the heart and its underlying mechanisms. MI was induced in male Sprague-Dawley rats through coronary artery ligation.

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Purpose: Renin-angiotensin-aldosterone system inhibitors (RAASi) are widely used in treatment of cardiovascular and renal disease. While effective, they pose a risk of hyperkalemia. In the general population, risk factors for hyperkalemia include chronic kidney disease, congestive heart failure, and use of medication affecting potassium balance.

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Primary aldosteronism is characterised by the excessive production of aldosterone, which is a key regulator of salt metabolism, and is the most common cause of secondary hypertension. Studies have investigated the association between primary aldosteronism and genetic alterations, with pathogenic mutations being identified. This includes a glycine-to-arginine substitution at position 151 (G151R) of the G protein-activated inward rectifier potassium (K) channel 4 (GIRK4), which is encoded by the gene.

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Evolution of mineralocorticoid receptor antagonists, aldosterone synthase inhibitors, and alternative treatments for managing primary aldosteronism.

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Department of Endocrinology, Metabolism, Rheumatology and Nephrology, Faculty of Medicine, Oita University, Oita, Japan.

Primary aldosteronism (PA) is a prevalent and curable secondary hypertensive disorder that accounts for 5-13% of all hypertension cases. The prevalence of resistant hypertension, cerebral and cardiovascular diseases, and renal complications is higher in PA patients than in those with essential hypertension. Appropriate diagnosis and treatment at an early stage may suppress cerebral and cardiovascular events.

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