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All Journal Heart Science Journal Riwayat: Educational Journal of History and Humanities
KURNIAWAN, ARY
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Humanities Education Health Professions Immunology & microbiology Medicine & Pharmacology Social Sciences

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Journal : Heart Science Journal

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The role of green tea and green coffee extract, empagliflozin and metformin treatment on FGF23 mRNA expression in calcified aorta tissue in metabolic syndrome model Sprague-Dawley rat Kurniawan, Ary; Mohammad Saifur Rohman; Yogibuana, Valerinna
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.2026.007.01.11

Abstract

Background: Metabolic syndrome (MetS), encompassing dyslipidemia, glucose intolerance, hypertension, and central obesity, increases cardiovascular risk, including vascular calcification. Fibroblast growth factor 23 (FGF23), a bone-derived regulator of phosphate and vitamin D, is implicated in vascular calcification in kidney disease, but its role in MetS-related calcification is unclear. Objective: To determine if MetS promotes vascular calcification and alters aortic FGF23 mRNA expression in rats, and to assess effects of green tea/coffee extract, metformin, and empagliflozin on FGF23 mRNA modulation. Methods: Twenty-five Sprague-Dawley rats were divided into five groups: negative control, MetS (induced via high-fat/high-sucrose diet and streptozotocin), and three treatment groups (green tea/coffee extract, metformin 500mg/kg, empagliflozin 30mg/kg). Aortic calcification (hematoxylin-eosin staining) and FGF23 mRNA expression (qRT-PCR) were analyzed after 9 weeks. ANOVA with LSD post-hoc tests was used. Results: This study found MetS induction promoted vascular calcification. FGF23 mRNA expression increased in the MetS group compared to controls, though not statistically significant. All treatments reduced FGF23 mRNA levels modestly, but effects lacked statistical significance (p = 0.851–0.989), likely due to complex, tissue specific regulation of FGF23. Conclusion: Metabolic disturbances in MetS may prime vascular tissues for calcification without significantly altering local FGF23 mRNA expression. Interventions targeting oxidative stress, inflammation, or glucose metabolism could modulate FGF23-related pathways, warranting further investigation into the underlying signaling mechanisms.
The role of FGF23 in cardiovascular disease: From pathophysiology to biomarker and therapeutic implications Kurniawan, Ary; Rohman, Mohammad Saifur
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.2026.007.01.4

Abstract

Cardiovascular disease (CVD) remains a leading global cause of mortality, necessitating deeper insights into non-traditional risk factors. Fibroblast growth factor 23 (FGF23), a hormone central to phosphate and vitamin D regulation, has emerged as a pivotal contributor to CVD pathogenesis. This review synthesizes evidence linking elevated FGF23 levels to adverse cardiovascular outcomes, including left ventricular hypertrophy, vascular calcification, hypertension, and atrial fibrillation in both chronic kidney disease (CKD) and individuals with preserved renal function. Mechanistically, FGF23 exerts direct effects on cardiac remodeling and calcium handling while indirectly promoting CVD via dysregulated mineral metabolism, renin-angiotensin-aldosterone system (RAAS) activation, and inflammatory pathways. Paradoxically, its compensatory rise in CKD to counteract hyperphosphatemia becomes maladaptive, accelerating cardiovascular pathology.  Despite its potential as a biomarker, challenges persist in establishing causality, disentangling confounding factors (e.g., inflammation, renal function), and developing targeted therapies that mitigate pathological effects without disrupting physiological phosphate homeostasis. Future research must prioritize defining context-specific FGF23 thresholds, elucidating cardiac versus systemic signaling mechanisms, and advancing receptor-specific interventions. Bridging these gaps will require multidisciplinary collaboration to translate FGF23’s dual roles, as both a compensatory hormone and a disease mediator into clinical strategies for CVD risk stratification and management.
Co-Authors Mohammad Saifur Rohman Yeni Rahmawati, Yeni Yogibuana, Valerinna