scholarly journals Understanding the Stony Bridge between Osteoporosis and Vascular Calcification: Impact of the FGF23/Klotho axis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Xu Wei ◽  
Xinyi Huang ◽  
Ning Liu ◽  
Baoyu Qi ◽  
Shengjie Fang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Vascular Calcification ◽  
Potential Role ◽  
Therapeutic Targets ◽  
Fibroblast Growth ◽  
Stiffness Ratio ◽  
Fgf 23 ◽  
The Relationship

A relationship between osteoporosis (OP) and vascular calcification (VC) is now proposed. There are common mechanisms underlying the regulation of them. Fibroblast growth factor- (FGF-) 23 and Klotho are hormones associated with the metabolic axis of osteovascular metabolism. Most recently, it was suggested that the FGF23-klotho axis is associated with increasing incidence of fractures and is potentially involved in the progression of the aortic-brachial stiffness ratio. Herein, we discussed the potential role of the FGF23/Klotho axis in the pathophysiology of OP and VC. We want to provide an update review in order to allow a better understanding of the potential role of the FGF23/Klotho axis in comorbidity of OP and VC. We believe that a better understanding of the relationship between both entities can help in proposing new therapeutic targets for reducing the increasing prevalence of OP and VC in the aging population.

Potential Role of Fibroblast Growth Factor in Enhancement of Fracture Healing

1998 ◽  
Vol 355S ◽  
pp. S283-S293 ◽  
Author(s):  
Michael L. Radomsky ◽  
Andrea Y. Thompson ◽  
Robert C. Spiro ◽  
James W. Poser
Keyword(s):  
Growth Factor ◽  
Fracture Healing ◽  
Fibroblast Growth Factor ◽  
Potential Role ◽  
Fibroblast Growth

scholarly journals Role of Fibroblast Growth Factor-23 in Coronary Slow Flow Phenomenon Pathogenesis

2021 ◽  
Vol 5 (4) ◽  
pp. 1029-1044
Author(s):  
Welly Oktaviandani ◽  
Taufik Indrajaya ◽  
Ali Ghanie ◽  
Erwin Sukandi
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Slow Flow ◽  
Fibroblast Growth ◽  
Flow Phenomenon ◽  
Coronary Slow Flow ◽  
Coronary Slow Flow Phenomenon ◽  
Fgf 23

The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.

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