Update on dyslipidemia in hypothyroidism

Hypothyroidism is often associated with elevated serum levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides. Thyroid hormone (TH) affects the production, clearance and transformation of cholesterol, but current research shows that thyroid-stimulating hormone (TSH) also participates in lipid metabolism independently of TH. Therefore, the mechanism of hypothyroidism-related dyslipidemia is associated with the decrease of TH and the increase of TSH levels. Some newly identified regulatory factors, such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiogenin-like proteins (ANGPTL), and fibroblast growth factors (FGF) are the underlying causes of dyslipidemia in hypothyroidism. High-density lipoprotein (HDL) serum concentration changes were not consistent, and its function was reportedly impaired. The current review focuses on the updated understanding of the mechanism of hypothyroidism-related dyslipidemia.

Improved myocardial performance in infarcted rat heart by injection of disulfide-cross-linked chitosan hydrogels loaded with basic fibroblast growth factor

Myocardial infarction (MI) has been considered as the leading cause of cardiovascular-related deaths worldwide. Basic fibroblast growth factor (bFGF) is a member of the fibroblast growth factors that promotes angiogenesis...

Progress on the study of fibroblast growth factors as novel therapeutics in post-stroke cognitive impairment

Post-stroke cognitive impairment (PSCI) is one of the most common complications after stroke, which severely affects the daily life abilities and social function of patients. Fibroblast growth factor (FGF), as a regulator of homeostasis, participates in the regulation of cell metabolism and hormone secretion, and can increase cerebral blood flow and promote nerve repair which improves PSCI. Here, we will conduct a review on the typing, characteristics, and mechanism of action of FGF to further understand its function and mechanism in PSCI

The Saga of Endocrine FGFs

Fibroblast growth factors (FGFs) are cell-signaling proteins with diverse functions in cell development, repair, and metabolism. The human FGF family consists of 22 structurally related members, which can be classified into three separate groups based on their action of mechanisms, namely: intracrine, paracrine/autocrine, and endocrine FGF subfamilies. FGF19, FGF21, and FGF23 belong to the hormone-like/endocrine FGF subfamily. These endocrine FGFs are mainly associated with the regulation of cell metabolic activities such as homeostasis of lipids, glucose, energy, bile acids, and minerals (phosphate/active vitamin D). Endocrine FGFs function through a unique protein family called klotho. Two members of this family, α-klotho, or β-klotho, act as main cofactors which can scaffold to tether FGF19/21/23 to their receptor(s) (FGFRs) to form an active complex. There are ongoing studies pertaining to the structure and mechanism of these individual ternary complexes. These studies aim to provide potential insights into the physiological and pathophysiological roles and therapeutic strategies for metabolic diseases. Herein, we provide a comprehensive review of the history, structure–function relationship(s), downstream signaling, physiological roles, and future perspectives on endocrine FGFs.

Muscle-tendon Crosstalk During Muscle Wasting

In organisms from flies to mammals, the initial formation of a functional tendon is completely dependent on chemical signals from muscle (myokines). However, how myokines affect the maturation, maintenance, and regeneration of tendons as a function of age is completely unstudied. Here we discuss the role of four myokines - fibroblast growth factors (FGF), myostatin, the secreted protein acidic and rich in cysteine (SPARC), and miR-29 - in tendon development and hypothesize a role for these factors in the progressive changes in tendon structure and function as a result of muscle wasting (disuse, aging and disease). Because of the close relationship between mechanical loading and muscle and tendon regulation, disentangling muscle-tendon crosstalk from simple mechanical loading is experimentally quite difficult. Therefore, we propose an experimental framework that hopefully will be useful in demonstrating muscle-tendon crosstalk in vivo. Though understudied, the promise of a better understanding of muscle-tendon crosstalk is the development of new interventions that will improve tendon development, regeneration, and function throughout the lifespan.

The Regenerative Potential of bFGF in Dental Pulp Repair and Regeneration

Regenerative endodontic therapy intends to induce the host’s natural wound-healing process, which can restore the vitality, immunity, and sensitivity of the inflammatory or necrotic pulp tissue destroyed by infection or trauma. Myriads of growth factors are critical in the processes of pulp repair and regeneration. Among the key regulatory factors are the fibroblast growth factors, which have turned out to be the master regulators of both organogenesis and tissue homeostasis. Fibroblast growth factors, a family composed of 22 polypeptides, have been used in tissue repair and regeneration settings, in conditions as diverse as burns, ulcers, bone-related diseases, and spinal cord injuries. Meanwhile, in dentistry, the basic fibroblast growth factor is the most frequently investigated. Thereby, the aim of this review is 2-fold: 1) foremost, to explore the underlying mechanisms of the bFGF in dental pulp repair and regeneration and 2) in addition, to shed light on the potential therapeutic strategies of the bFGF in dental pulp–related clinical applications.

Modern treatment of infantile hemangioma

Infantile hemangioma (IH) is the most common benign vascular tumor in children of the first year, which is based on abnormal proliferation of endothelial cells under the influence of the main pro-angiogenic factors: vascular endothelial growth factor (VEGF) and fibroblast growth factors (FGF). It develops in the first weeks after birth, forming over 3–9 months with regression in the next 3–7 years. Three-quarters of infantile hemangiomas are nodular and are not accompanied by malformations. At the same time, segmental IH is most often associated with syndromic forms. Despite spontaneous regression (in 90% of cases), some forms and localization of IH can lead to the development of complications, local and endangering vital functions. In most cases, the diagnosis is based on anamnesis, characteristic features of the tumor, and clinical course. Additional studies (ultrasound DG, MRI/CT, biopsy) are necessary in complicated forms and in doubtful clinical cases.

MO577EXPANDING THE POTENTIAL BENEFITS OF FERRIC CITRATE FOR IMPROVING IRON-DEFICIENCY ANAEMIA AND MINERAL BONE DISORDER PARAMETERS IN NON-DIALYSIS-DEPENDENT CHRONIC KIDNEY DISEASE PATIENTS: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS

Background and Aims Most of non-dialysis-dependent chronic kidney disease (NDD-CKD) patients will suffer from iron-deficiency anaemia (IDA) also mineral and bone disorders (CKD-MBD) as consequences of CKD progression. Ferric citrate (FC) is an iron-based phosphate binder that based on previous studies showed efficacies in improving IDA and CKD-MBD parameters although the results were still inconclusive. This study aims to establish the overall efficacies of FC in improving IDA and CKD-MBD parameters in NDD-CKD patients. Method We did comprehensive searching using predefined keywords in online databases of Pubmed, EMBASE, ScienceDirect, and The Cochrane Library, to include all relevant studies from 2000-2020. We included all randomized controlled trials (RCTs) accessing the efficacies of FC in improving IDA and CKD-MBD parameters compared with standard care (SC) in NDD-CKD patients. The CKD-MBD parameters analysed in this study are changes in serum phosphorus (P), serum calcium ions (Ca), alkaline phosphatase (ALP), intact fibroblast growth factors-23 (iFGF-23), C-terminal fibroblast growth factors-23 (cFGF-23), and intact parathyroid hormone (iPTH), while the IDA parameters analysed are changes of haemoglobin (Hb), serum iron (Fe), transferrin saturation (TSAT), and ferritin. Bias risk was accessed by using the revised Cochrane Risk-of-bias (RoB-2) tool. Analysis was performed to provide standard mean difference (SMD) with 95% confidence interval (CI) using random-effect heterogeneity test. Results We included six RCTs with total of 1,082 participants met our inclusion criteria. The FC significantly improve CKD-MBD parameters of P (SMD = -0.84. 95% CI = -1.21 to -0.07, p<0.00001, I2 = 74%), iFGF-23 (SMD = -0.43. 95% CI = -0.73 to -0.13, p = 0.005, I2 = 73%), cFGF-23 (SMD = -0.74. 95% CI = -1.12 to -0.35, p = 0.0002, I2 = 78%), and iPTH (SMD = -0.23. 95% CI = -0.40 to -0.06, p = 0.008, I2 = 0%), while the improvement of Ca (SMD = 0.16. 95% CI = -0.07 to 0.38, p = 0.17, I2 = 0%) and ALP (SMD = 0.03. 95% CI = -0.22 to 0.28, p = 0.81, I2 = 14%) are not statistically significant compared with the SC group. The FC also significantly improve IDA parameters of Hb (SMD = 1.10. 95% CI = 0.06 to 2.14, p = 0.04, I2 = 97%), TSAT (SMD = 1.18. 95% CI = 0.67 to 1.69, p<0.00001, I2 = 72%), and ferritin (SMD = 1.10. 95% CI = 0.34 to 1.86, p = 0.004, I2 = 87%) compared with the SC group, unless the improvement of Fe is not statistically significant (SMD = 1.34. 95% CI = -0.28 to 2.95, p = 0.11, I2 = 97%). Conclusion The ferric citrate shows potential benefits for improving iron-deficiency anaemia and CKD-MBD parameters in NDD-CKD patients. Nevertheless, further trials are needed to establish the efficacies.