China 
Africa 
Explore chapters and articles related to this topic
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
There are many mediators secreted by inflammatory cells and have been hypothesized to play role in the pathogenesis of SSc. Adipokines, chemical mediators synthesized by adipocytes, such as adiponectin, visfatin, retinol binding protein-4, apelin, and resistin, have demonstrated a potential role in the pathogenesis of SSc. Resistin, also secreted by inflammatory cells, triggers proliferative response in vascular smooth muscles resulting in angiogenesis in pulmonary vasculature. The significant increase in serum levels of resistin has been found in patients with SSc.27
Nutrition and Nutraceutical Supplements for the Treatment of Hypertension
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
l-arginine and endogenous methylarginines are the primary precursors for the production of nitric oxide (NO), which has numerous beneficial cardiovascular effects, mediated through conversion of l-arginine to NO by eNOS. Patients with hypertension, hyperlipidemia, DM, and atherosclerosis have increased levels of HS-CRP and inflammation; increased microalbumin; low levels of apelin (stimulates NO in the endothelium); increased levels of arginase (breaks down arginine); and elevated serum levels of ADMA, which inactivates NO.131–135
Carriers for Nucleic Acid Delivery to the Brain
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Sequence-defined oligoaminoamide oligomers were used for receptor-mediated delivery of siRNA [101] and pDNA [102] into glioma in vivo after systemic injection. For siRNA delivery, an untargeted lipo-oligomer was mixed with a PEGylated oligomer containing an angiopep-2 ligand targeting the LRP-1 receptor, which is overexpressed both on the surface of BCECs and glioma cells [101]. A similar cascade-targeting strategy was used for the delivery of therapeutic pDNA. Here, a nontargeted oligomer was mixed with a PEGylated oligomer containing the heptapeptide I6P7, which binds the interleukin 6 receptor (IL6R). IL6R expression was detected both on the tumour BBB and in various brain tumours such as glioblastoma (Fig. 9.3). Targeted delivery of pDNA encoding inhibitor of growth 4 (pING4) significantly prolonged the survival time of orthotopic U87 glioma-bearing mice [102]. Reporter gene expression was found in the brains of U87 glioblastoma-bearing mice after intracranial injection of pDNA polyplexes formed with bioreducibly linked (cRGDyK)-PEG-ss-PEI. The Arg-Gly-Asp (RGD) sequence binds integrin receptors which are highly expressed in glioma cells, while the cyclic RGD peptide cRGDyK is known to increase the affinity and selectivity of the receptor by providing conformational restraint [32, 103]. PEGPEI polyplexes carrying the therapeutic gene pORF-hTRAIL were targeted with a protease-resistant retro-enantio C-end rule (CendR) peptide-binding neuropilin-1, which plays an important role in tumour angiogenesis, growth and metastasis [104]. Intravenous injection of the polyplexes significantly prolonged the survival time of intracranial U87 glioma-bearing mice from 25 to 30 days. Epidermal growth factor receptor (EGFR)-targeted intratumoural delivery of the synthetic antiproliferative double-stranded RNA polyinosine-cytosine (poly IC) formulated with PEI-PEG-EGF [105–107] induced the complete regression of intracranial tumours in mice, with no obvious adverse toxic effects on normal brain tissue [105]. Several preclinical studies explore the delivery of siRNAs to target genes involved in gliomagenesis, tumour progression and therapy resistance of glial tumours [99]. Tumour growth inhibition and prolonged survival of animals was found after both local application [108–114] and systemic injection [115–120] of siRNA nanoparticles (Table 9.1). Another potentially promising target for glioma-directed delivery of therapeutics is the proangiogenic apelin receptor (APLNR) and its cognate ligand apelin, which play a central role in controlling glioblastoma vascularisation [121]. Apelin and APLNR were found to be dramatically upregulated in glioblastoma-associated microvascular proliferations, but not in the healthy brain [122].
Plasma visfatin and apelin levels in adolescents with polycystic ovary syndrome
Published in Gynecological Endocrinology, 2023
Xiangyan Ruan, Meng Li, Min Min, Rui Ju, Husheng Wang, Zhongting Xu, Suiyu Luo, Alfred Otto Mueck
In terms of apelin, current research conclusions differ greatly regarding its relationship to PCOS. Some studies have found significantly increased apelin levels in PCOS patients [22,23]. Contrary to this, Chang et al. [24] and Altinkaya et al. [25] have found apelin levels in PCOS patients were lower when compared to controls. However, Benk et al. [26] and Olszanecka Glinianowicz et al. [27] found no differences in apelin levels between PCOS patients and controls. In our study, there was no difference in apelin levels between adolescent PCOS patients and controls. Recently, it has been suggested that apelin can enhance insulin sensitivity and improve insulin resistance [28]. In addition, it has been shown that apelin can regulate lipid metabolism by up-regulating PI3K/Akt signal pathway, and play a role in reducing CHO-concentrations and increasing HDL-C levels [29]. We found that apelin was only positively correlated with HDL-C in the control-group. In our PCOS patients, there was no difference in apelin with or without IR, and there was no correlation between apelin and various relevant PCOS indicators. This may be due to the small sample size of our study, or a minor role of apelin in the glucose and lipid metabolism in PCOS. There may also be differences due to race, age, genetic characteristics, eating habits, etc., which need further exploration in the future.
Effects of acute endurance exercise on follistatin-like 1 and apelin in the circulation and metabolic organs in rats
Published in Archives of Physiology and Biochemistry, 2022
Michihiro Kon, Yuko Tanimura, Hideo Yoshizato
The present study demonstrated the increase in the circulating levels of apelin at immediately after a single bout of endurance exercise, consistent with previous findings investigating the effect of acute exercise on the concentration of plasma apelin (Bilski et al. 2016, Kon et al. in press). In contrast, a single bout of endurance exercise did not affect the expression of apelin in skeletal muscle, adipose, heart, and liver tissues in this study, suggesting that the elevation in the levels of circulating apelin due to a single bout of endurance exercise might not be derived from the metabolic tissues that this study investigated. A previous study has demonstrated that aside from adipose tissues, higher expressions of apelin were also noted in kidney tissue (Boucher et al. 2005). Therefore, an investigation regarding the impacts of acute endurance exercise on the expression of apelin in other organs including kidney may be required in the future.
Effects of acute sprint interval exercise on follistatin-like 1 and apelin secretions
Published in Archives of Physiology and Biochemistry, 2021
Michihiro Kon, Yoshiko Ebi, Kohei Nakagaki
In recent years, skeletal muscle tissue has been recognized as an important secretion source of cytokines (hence, named myokines) such as interleukin (IL)-6 and IL-15 (Pedersen and Febbraio 2008). Follistatin-like 1 (FSTL1) (Lee et al. 2017) and apelin (Dray et al. 2008, Yue et al. 2010) are novel myokines that have recently been indicated as being related to glucose metabolism in skeletal muscle. FSTL1 is a secreted glycoprotein belonging to a member of the follistatin family (Sumitomo et al. 2000). In an in vitro study using skeletal muscle cells, FSTL1 stimulated GLUT4 translocation into the plasma membrane and increased glucose uptake (Lee et al. 2017). Apelin, which is a novel bioactive peptide hormone, presented and secreted from various tissues including skeletal muscle (Tatemoto et al. 1998). Dray et al. (2008) have demonstrated that intravenous injection of apelin enhanced glucose utilization in skeletal muscle. In addition, knocking out apelin impaired insulin sensitivity and decreased insulin sensitivity was improved by exogenous administration of apelin (Yue et al. 2010). These results suggest that FSTL1 and apelin are related to glucose metabolism in skeletal muscle and have improvement effect against insulin sensitivity. Although FSTL1 and apelin may be associated with the SIT-induced improvement effects on glucose metabolism and insulin sensitivity, the effect of SIT on FSTL1 and apelin secretions has not been examined.