<scp>FGF</scp>‐23 dysregulates calcium homeostasis and electrophysiological properties in <scp>HL</scp>‐1 atrial cells

Kao, Yu Hsun; Chen, Yao Chang; Lin, Yung Kuo; Shiu, Rong Jie; Chao, Tze Fan; Chen, Shih Ann; Chen, Yi Jen

doi:10.1111/eci.12296

Cited by 32 publications

(28 citation statements)

References 34 publications

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“…Consistent with these observations, elegant experiments in animal models have documented direct effects of FGF23 to promote hypertrophy, contractility and arrhythmic potential of the myocardium (10–12). Additional studies have found indirect adverse cardiac effects of FGF23, such as activation of the renin-angiotensin system and promotion of sodium reabsorption in the distal tubule of the kidney (13–15).…”

Section: Introductionmentioning

confidence: 64%

Epidemiologic insights on the role of fibroblast growth factor 23 in cardiovascular disease

Scialla

2015

Current Opinion in Nephrology and Hypertension

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Purpose of Review Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D homeostasis and rises as kidney function declines. Animal studies have demonstrated direct and indirect effects of FGF23 that may promote heart disease. Herein we review the recent epidemiologic literature evaluating the relationship between FGF23 and cardiovascular disease. Recent Findings In observational prospective studies higher FGF23 associates with greater risk of incident cardiovascular disease including ischemic heart disease, stroke, heart failure, and atrial fibrillation. These studies establish a temporal sequence of events over long term-follow up that suggest a possible role of FGF23 in cardiovascular disease pathogenesis. In most studies risk is generally graded, however in the largest study to date, higher FGF23 within the low-normal range was not associated with higher risk. In several recent studies higher FGF23 associated more strongly with risk of congestive heart failure compared with atherosclerotic events, a finding consistent with surrogate endpoints and animal experiments. Currently the utility of FGF23 as a predictive biomarker of cardiovascular risk is not established, and interventions to reduce FGF23 need to be studied to confirm its possible pathophysiologic role. Summary Higher FGF23 is associated with the subsequent development of cardiovascular disease, and perhaps most notably heart failure, in a growing number of studies. These findings bolster ongoing efforts to lower FGF23 using strategies to reduce phosphate intake and absorption.

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Section: Introductionmentioning

confidence: 64%

Epidemiologic insights on the role of fibroblast growth factor 23 in cardiovascular disease

Scialla

2015

Current Opinion in Nephrology and Hypertension

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“…Previous studies have shown that inflammation or anti-inflammation can change heart rates through regulation on oxidative stress and autonomic nervous system [39][40][41][42] . Moreover, recent studies indicate that FGF-23 increased cardiac electrical activities by modulating calcium homeostasis [43,34] . Therefore, the attenuating effects of MPT0E014 on cardiac inflammation and FGFR-1 may result in the slowing of heart rates in MPT0E014-treated HF rats, at least in part.…”

Section: Discussionmentioning

confidence: 99%

Novel Histone Deacetylase Inhibitor Modulates Cardiac Peroxisome Proliferator-Activated Receptors and Inflammatory Cytokines in Heart Failure

et al. 2015

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Background: Heart failure (HF) affects cardiac metabolism and inflammation. Histone deacetylases (HDACs) play a critical role in cardiac pathophysiology. This study investigated whether HDAC inhibition can regulate HF by modifying cardiac inflammation and peroxisome proliferator-activated receptor (PPAR) isoforms. Methods: Echocardiography, electrocardiography, ELISA and Western blot were performed in rats with isoproterenol-induced HF, with and without orally administered MPT0E014 (a novel HDAC inhibitor, 50 mg/kg for 7 consecutive days). Results: The left ventricles (LVs) of HF rats expressed significantly higher levels of HDAC1, HDAC2, HDAC3, HDAC4 and HDAC6 than the healthy LVs did. HF rats treated with MPT0E014 exhibited improved cardiac fraction shortening with reducing chamber size. The MPT0E014-treated HF LVs exhibited a smaller increase in the expression of interleukin (IL)-6, p22, SMAD2/3, extracellular signal-regulated kinase 1/2, PPAR isoforms and circulatory tumor growth factor-β1 than the untreated HF LVs did. Moreover, MPT0E014-treated HF LVs expressed less fibroblast growth factor receptor than untreated HF LVs did. Conclusions: HDAC inhibition can improve cardiac function and attenuate the effects of HF on cardiac metabolism and inflammation, which might contribute to the beneficial effects of HDAC inhibition in HF.

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“…FGF23 reduction is another potential benefit of treatment with non-CBPBs. Elevated levels of FGF23 appear to influence cardiac fibrosis, hypertrophy and arrhythmogenic potential through calcium dysregulation [16,17], and higher levels have been associated with greater risks for death and progression to dialysis in patients with CKD stages 2-4 [18]. FGF23 reductions have been reported in CKD stages 3-4 after treatment with sevelamer hydrochloride over 6 weeks [19] and ferric citrate over 12 weeks [20], and in CKD stages 4-5 after treatment with lanthanum over 4 months [21].…”

Section: T H E B I G Q U E S T I O N : I S T H E R E a C A S E F O R mentioning

confidence: 99%

Calcium-based phosphate binders; down, but not out

Elder

2017

Nephrology Dialysis Transplantation

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FGF‐23 dysregulates calcium homeostasis and electrophysiological properties in HL‐1 atrial cells

Abstract: FGF-23 increases HL-1 cells arrhythmogenesis with calcium dysregulation through modulating calcium-handling proteins.

Cited by 32 publications

References 34 publications

Epidemiologic insights on the role of fibroblast growth factor 23 in cardiovascular disease

Epidemiologic insights on the role of fibroblast growth factor 23 in cardiovascular disease

Novel Histone Deacetylase Inhibitor Modulates Cardiac Peroxisome Proliferator-Activated Receptors and Inflammatory Cytokines in Heart Failure

Calcium-based phosphate binders; down, but not out

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