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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
One of the recently identified mechanisms regulating TGF-β signaling in the endothelium involves FGF-mediated suppression of TGF receptor expression. Baseline FGF signaling is responsible for the maintenance of let-7 miRNA expression in normal endothelial cells. Let-7 miRNAs target expression of a number of TGF family members, including TGFR1; in the absence of FGF input, let-7 levels decline and TGFR1 levels increase, thus enabling activation of TGF-β signaling.437 The importance of this FGF/TGF signaling link lies in the fact that the continuous FGF signaling input needed to suppress TGF-β signaling activation depends on expression of the key endothelial FGF receptor, FGFR1.437 Interestingly, certain inflammatory conditions associated with production of TNF-α, interleukin 1β, or interferon-γ result in a profound decline of FGFR1, activation of TGF-β signaling, and the onset of EndMT (Figure 2.18). Thus, this mechanism likely explains the previously reported link between inflammation and EndMT.438,457–459 Atherosclerosis, a chronic inflammatory disease potentiated by TNF-α460 and interferon-γ,461 is associated with infiltration of T cells and macrophages into diseased blood vessel wall; thus, EndMT may well be an important contributor to altered cellular and ECM composition in the vessel wall that promotes atherosclerotic disease progression of low T cells. It is also maybe the key contributor to peripheral, cerebral, and coronary vasculitis, which can result in simple fibrosis resulting in scar tissue.
Craniofacial Regeneration—Bone
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Laura Guadalupe Hernandez, Lucia Pérez Sánchez, Rafael Hernández González, Janeth Serrano-Bello
Most recognizable craniofacial syndromes are monogenic Mendelian disorders, different mutations in the same gene. However, it is not a rule because, more than 7000 single-gene disorders have been identified in craniofacial disorders such as Stickler syndrome and the craniosynostosis syndromes involving different FGFR genes (FGFR1, FGFR2, FGFR3).
Exercise training increases the S-Klotho plasma levels in sedentary middle-aged adults: A randomised controlled trial. The FIT-AGEING study
Published in Journal of Sports Sciences, 2019
F. J. Amaro-Gahete, A. De-la-O, L. Jurado-Fasoli, A. Espuch-Oliver, T. de Haro, A. Gutierrez, J. R. Ruiz, M. J. Castillo
Three Klotho gene products have been identified: α-Klotho (which is expressed in distal convoluted tubules in the kidney, parathyroid and choroid plexus in the brain), β-Klotho (which control the bile acids, lipid and energy metabolism together with FGF15/19, and FGF21) and γ-Klotho (which is involved in brown adipose tissue metabolism) (Hu, Shiizaki, Kuro-O, & Moe, 2013; Kim, Hwang, Park, Kong, & Cha, 2015). They share a substantial degree of homology, but they also seem to have different physiological actions (Hu et al., 2013; Kim et al., 2015). The α-Klotho gene encodes a type 1 single-pass transmembrane glycoprotein (M Kuro-O et al., 1997). The intracellular domain is short and non-functional (Kim et al., 2015). The extracellular domain, however, forms a complex with fibroblast growth factor 23 and fibroblast growth factor receptor 1 (Kim et al., 2015) and has a potential site for proteolytic cleavage (Bloch et al., 2009; Chang et al., 2005). The cleaved Klotho is commonly known as secreted Klotho (S-Klotho), and it is detected in blood, urine, and cerebrospinal fluid (Imura et al., 2004; Kurosu et al., 2005). S-Klotho can act as a soluble paracrine or endocrine mediator through the modulation of the action of growth factors and cytokines such as insulin, insulin-like growth factor-I (acting as a suppressor of tyrosine phosphorylation of insulin and insulin-like growth factor-I receptors, which results in reduced activity of insulin receptor substrate proteins and their association with phosphoinositide 3-kinases, thereby inhibiting insulin and insulin-like growth factor-I signalling), transforming growth factor-β (TGF-β), Wnt signalling, and gamma interferon (IFNγ), which are associated with cell senescence and the aging process in mice (Doi et al., 2011; Imura et al., 2004; Kim et al., 2015). Indeed, higher S-Klotho plasma levels have been associated with improved survival in chronic kidney disease patients (Sakan et al., 2014), and lower levels have been related to increased cardiovascular disease incidence in adults (Semba et al., 2011) and all-cause mortality in chronic haemodialysis patients (Otani-Takei et al., 2015).