China
Africa
Explore chapters and articles related to this topic
Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
RANKL binds to the osteoclast cell-surface receptor RANK. Subsequently, RANK is trimerized and recruits a member of the TNF receptor-associated factors (TRAFs) at specific sites within its cytoplasmic domain (167). These factors are TRAF 2, 5, and 6. The most basic factor for osteoclasts (precursors and mature) seems to be TRAF 6 (56,168). The signaling pathways that are activated after the binding of RANK with TRAF are as follows: Four pathways that induce the formation of osteoclasts: (a) inhibitor of NF-κB kinase (IKK)/NF-κB), (b) nuclear factor of activated T cells (NFATc1), (c) c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1), and (d) c-myc.Three pathways that mediate activation ([a] MKK6/p38/MITF and [b] Src) and survival of osteoclasts ([a] kinase pathway regulated by extracellular signal and [b] Src pathway) (169). Figure 2.2a summarizes the signal transduction pathways after RANK.
The Renin—Angiotensin—Aldosterone System
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Ulrike M. Steckelings, Thomas Unger
ACE can act as a receptor itself in that the intracellular tail is phosphorylated upon binding of ACE inhibitors and bradykinin (but not Ang I) (24). Ligand binding increases the activity of ACE-associated c-Jun N-terminal kinase (JNK) and elicits the accumulation of phosphorylated c-Jun in the nucleus.
Postimplantation diabetic embryopathy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Ulf J. Eriksson, Parri Wentzel
Several enzyme systems have been reported as disturbed in the offspring of diabetic animals, and, consequently, have been assumed to be part of the teratogenic process. The two most often reported are varied activation/inhibition of PKC isoforms162,190–195 and activation of c-Jun N-terminal kinases (JNKs) (Table 41.4).196–200
The mechanism of triptolide in the treatment of connective tissue disease-related interstitial lung disease based on network pharmacology and molecular docking
Published in Annals of Medicine, 2022
Wen Zhu, Yehui Li, Junjie Zhao, Yifan Wang, Yixi Li, Yue Wang
First of all, These potential targets are closely associated with the progression of pulmonary fibrosis. For example, STAT3 controls crosstalk between epithelial cells and fibroblasts which in turn contributes to disease progression [31]. In fibrogenesis, IL-6 can promote the phosphorylation of STAT3 and its translocation to the nucleus for further gene transcription [32]. JAK2 and STAT3 were verified as a hub pathway to modulating oxidative stress, inflammation, and cell apoptosis in a model of bleomycin-induced acute lung injury rat [33]. c-Jun-N-terminal kinase 1 (JNK1) [34] signalling pathways play an essential role in various physiological and pathological processes such as cell cycle, reproduction, apoptosis, and cellular stress. Recently, it has been found that the transcription factor JUN is highly expressed in pulmonary fibrosis, and its overexpression in mice can induce pulmonary fibrosis. During BLM injury, the pro-inflammatory cytokine such as IL-17A will be up-regulated and mediate the inflammation in the alveolar epithelial cell and also brings about recruitment of certain inflammatory cells in the alveolar surface. IL-17A-mediated p53-fibrinolytic aspects are involved in the regulation of pathogenic progression of acute lung injury (ALI) and pulmonary fibrosis [35].
Paeonol attenuates heart failure induced by transverse aortic constriction via ERK1/2 signalling
Published in Pharmaceutical Biology, 2022
Xu Chen, Zhiyu Zhang, Xiaowei Zhang, Zhi Jia, Jun Liu, Xinpei Chen, Aiqing Xu, Xue Liang, Guangping Li
Previous studies have demonstrated that members of mitogen-activated protein kinase (MAPK) family play a vital role in intracellular and extracellular signal transduction in different cells and regulate the important biological process, including differentiation, proliferation, migration and apoptosis (Sun et al. 2015). The progression of apoptosis under pathological conditions of myocardial ischaemia was accompanied by the activation of ERK1/2 signalling pathway (Yan et al. 2018). C-Jun N-terminal kinase (JNK) is thought to be involved in the induction of apoptosis by activating the cellular damage signalling pathway. JNK signalling pathway can be activated by inflammation, contributing to the terminal point of HF from transverse aortic constriction (TAC) to cardiac remodelling. Some studies have confirmed that the regulation of the JNK/Bcl-2 pathway may be the key mechanism of anthocyanin in alleviating myocardial infarction (Syeda et al. 2019). Based on a growing body of research, we hypothesized that the ERK1/2/JNK signalling pathway is involved in the development of TAC-induced HF.
The Role of C-Jun N-terminal Kinase-1 in Controlling Aquaporin-1 and Choroidal Thickness during Recovery from Form-deprivation Myopia in Guinea Pigs
Published in Current Eye Research, 2021
Wei Chen, Zhiwei Li, Qimiao Wang, Yan Wang, Yue Zhang
C-Jun N-terminal kinase-1 (JNK1) is an important member of the mitogen-activated protein kinase family. The JNK signaling pathway can be activated by growth factors, cytokines, environmental stress (UV, cell hyperosmotic pressure, ischemia-reperfusion injury), and other stimulating signals to regulate the transcription of downstream genes.10 Recent study have shown that the mRNA level of mapk8ip3 (a factor that can cause JNK signal pathway activation) decreased during the development of myopia, and the levels of downstream genes of JNK, such as c-fos, was also reduced.11 In a previous study on AQP1 activation, Umenishi F et al. found that the expression of AQP-1 increased after activation of JNK in rat bone marrow cells and decreased after inhibition of JNK,12 indicating that the JNK pathway can affect AQP1 activation. Whether JNK1 regulates AQP-1 during the recovery from myopia has not been studied. We speculate that changes in the JNK1 signaling pathway may lead to the changes in AQP-1 content and CT, thus influencing the recovery from myopia.