China
Africa
Explore chapters and articles related to this topic
Role of Oxidative Stress in the Onset of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Tasnuva Sarowar, Md. Hafiz Uddin
Abeta has a dual role on cellular protection. At picomolar level, abeta exerts cellular protection against oxidative stress and enhances hippocampal long-term potentiation (LTP) (Puzzo et al. 2008), whereas higher concentration of abeta is toxic by itself. Application of external abeta increases the oxidative stress in vitro (Behl et al. 1994). In various animal models of AD, age-associated accumulations of abeta correlates with elevated hydrogen peroxide and nitric oxide production (Smith et al. 1998). Further, oxidative stress enhances the production of abeta via c-Jun N-terminal kinase (JNK) pathway. JNK is stimulated by oxidative stress and increases the expression and activity of beta and gamma secretases (Tamagno et al. 2008, Shen et al. 2008). Additionally, oxidative stress has been proven to enhance abeta production in various mouse models (Li et al. 2004, Nishida et al. 2006). Thus, abeta production and oxidative stress are interlinked in the pathology of AD.
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.
Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy
Published in Renal Failure, 2023
Zhongdi Liu, Yifan Chen, Zhe Du, Fengxue Zhu, Wei Huang
Previous researches have confirmed that autophagy may play different roles in different renal diseases, different renal cell types, and different stages of disease progression, and the detailed regulatory mechanism and signal transmission remain to be further clarified. Recent studies have shown that autophagy is associated with the intracellular accumulation of reactive oxygen species (ROS) in response to environmental stresses, such as starvation, infection, and various diseases. During LIR, the release of a large number of oxygen free radicals leads to the accumulation of ROS in cells. As signaling molecules, ROS induce autophagy by activating c-Jun N-terminal kinase (JNK) and adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signal transduction pathways or by inhibiting Akt-mTOR and other pathways [35]. It was demonstrated that autophagy can phagocytose lysosomes and restore lysosomal function to prevent cell damage. Autophagy could also inhibit the activity of inflammasomes by removing damaged organelles and regulating the inflammatory response to prevent the production of inflammatory cytokines [36]. However, overactivated autophagy could induce inflammatory responses, resulting in cell and tissue damage, and even organ dysfunction [37]. It has been reported that autophagy was involved in the development of renal ischemia and reperfusion injury, since numerous experiments demonstrated the activation of autophagy during renal ischemia and reperfusion injury [33]. However, it is still under debate whether the upregulation of autophagy has a protective effect on the kidney or exacerbates kidney damage.
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.
miR-128 regulated the proliferation and autophagy in porcine adipose-derived stem cells through targeting the JNK signaling pathway
Published in Journal of Receptors and Signal Transduction, 2021
Pengfei Gao, Haizhen Wang, Juan Liu, Yiqi Wu, Wei Hei, Zhiqiang He, Chunbo Cai, Xiaohong Guo, Guoqing Cao, Bugao Li
The c-Jun N-terminal kinase (JNK) signaling plays an important role in inflammation and apoptosis [11]. JNKs have a close relationship with c-Jun which is a kind of phosphorylation-activated transcription factor. JNKs consist of three encoded genes Jnk1, Jnk2 and Jnk3 in human. Jnk1 and Jnk2 are highly expressed in human tissues and Jnk3 is mainly expressed in the brain, heart and testis tissues. JNKs can be triggered by a variety of stressors such as oxidative stress and ultraviolet (UV) irradiation, resulting in cell apoptosis and growth inhibition [12]. Translation of JNK proteins from cytoplasm to nucleus induces activation of c-Jun [13], thus regulating the expression of apoptosis related genes, including B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) [14,15]. The JNK pathway is also the target of miRNAs [16,17]. However, the effects of miR-128-JNK on porcine adipose-derived stem cells (ASCs) remain uncertain.