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All Journal Journal of Biomedicine and Translational Research Heart Science Journal
Taufiq, Fikri
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Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology

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Hyperuricemia as a Risk Factor for Cardiovascular Diseases Hisatome, Ichiro; Li, Peili; Taufiq, Fikri; Maharani, Nani; Kuwabara, Masanari; Ninomiya, Haruaki; Bahrudin, Udin
Journal of Biomedicine and Translational Research Vol 6, No 3 (2020): December2020
Publisher : Faculty of Medicine, Universitas Diponegoro

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14710/jbtr.v6i3.9383

Abstract

Serum uric acid level above 7 mg/dl is defined as hyperuricemia, which gives rise to the monosodium urate (MSU), causing gout and urolithiasis. Hyperuricemia is an independent risk factor as well as a marker for hypertension, heart failure, atherosclerosis, atrial fibrillation, and chronic kidney disease. MSU crystals, soluble uric acid (UA), or oxidative stress derived from xanthine oxidoreductase (XOR) might be plausible explanations for the association of cardio-renovascular diseases with hyperuricemia. In macrophages, MSU activates the Nod-like receptor family, pyrin　domain containing 3(NLRP3) inflammasome, and proteolytic processing mediated by caspase-1 with enhanced interleukin (IL)-1β and IL-18 secretion. Soluble UA accumulates intracellularly through UA transporters (UAT) in vascular and atrial myocytes, causing endothelial dysfunction ad atrial electrical remodeling. XOR generates reactive oxygen species (ROS) that lead to cardiovascular diseases. Since it remains unclear whether asymptomatic hyperuricemia could be a risk factor for cardiovascular and kidney diseases, European and American guidelines do not recommend pharmacological treatment for asymptomatic patients with cardio-renovascular diseases. The Japanese guideline, on the contrary, recommends pharmacological treatment for hyperuricemia with CKD to protect renal function, and it attaches importance of the cardio-renal interaction for the treatment of asymptomatic hyperuricemia patients with hypertension and heart failure.
The impact of combined decaffeinated green coffee and green tea, metformin, and empagliflozin on SAMD11 mRNA expression in vascular calcification associated with metabolic syndrome in Sprague Dawley rats Taufiq, Fikri; Saifur Rohman, Mohammad; Fuji Rahimah, Anna
Heart Science Journal Vol. 7 No. 1 (2026): Accelerating Clinical Breakthroughs: The Journey from Molecular Discovery to Pa
Publisher : Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.hsj.2026.007.01.9

Abstract

Background: Vascular calcification, a common complication of metabolic syndrome, increases cardiovascular risk, and SAMD11 may be implicated in its development. Improving blood glucose with metformin, empagliflozin or a combination of decaffeinated green tea and green coffee may improve metabolic syndrome which may ultimately lead to SAMD11 expression. However, the precise mechanisms by which SAMD11 play a role on vascular calcification in metabolic syndrome remain unknown. Objective: This study investigated the effect of combined decaffeinated green coffee and green tea, metformin and empagliflozin on SAMD11 mRNA expression in metabolic syndrome-induced vascular calcification. Methods: Twenty-five 12-week-old male Sprague Dawley (SD) rats were randomly assigned to five groups: control, metabolic syndrome (MetS), combine decaffeinated green tea 300 mg/kgBW and green coffee 200 mg/KgBW treatment, metformin 500 mg/kgBW treatment, and empagliflozin 30 mg/KgBW treatment. MetS was induced using established procedures. Vascular calcification and aortic SAMD11 mRNA expression were assessed via HE staining and RT-PCR, respectively. Result: Induction of metabolic syndrome in SD rats successfully led to vascular calcification. Metabolic syndrome induction significantly increased SAMD11 mRNA expression (p=0.018), an effect that was reversed by treatment with metformin (p=0.002) and empagliflozin (p=0.005). While a combination of decaffeinated green tea and green coffee showed a reduction in SAMD11 mRNA expression, but this reduction was not statistically significant (p=0.066). Conclusion: Metabolic syndrome may promote vascular calcification by enhancing SAMD11 mRNA expression. Controlling hyperglycaemia, a characteristic of metabolic syndrome, with metformin and empagliflozin, reduced SAMD11 mRNA expression. Potential hyperglycaemic control by decaffeinated green tea and green coffee did not changes SAMD11 mRNA expression.
Co-Authors Fuji Rahimah, Anna Hisatome, Ichiro Kuwabara, Masanari Li, Peili Nani Maharani Ninomiya, Haruaki Saifur Rohman, Mohammad Udin Bahrudin, Udin