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Responses to Muscular Exercise, Heat Shock Proteins as Regulators of Inflammation, and Mitochondrial Quality Control
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Alex T. Von Schulze, Paige C. Geiger
As mentioned previously, HSP induction occurs as a cellular stress response to stimuli such as exercise or oxidative stress. This induction is first initiated by the primary transcription factor for HSPs, heat shock factor 1 (HSF1), which trimerizes and undergoes nuclear translocation under stress (53, 78). In combination with the transcriptional co-activator peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), HSF1 binds to its canonical DNA docking sites known as heat shock elements (HSEs), which act as promoter regions for HSP-related genes (78, 97). Upon the HSF1–PGC1α complex binding, HSF1 is phosphorylated and transcription is initiated (78). As with many other proteins, HSF1's activity is dependent on HSP content. Specifically, once enough HSPs (specifically HSP70) are translated, they in turn bind to HSF1, removing it from its DNA docking site and returning it to its monomeric form in the cytoplasm (78). PGC1α can also counter-regulate HSF1 through transcriptional repression (60). In this way, the stress response is a tightly regulated process coupled to cellular HSP and PGC1α content. Moreover, this increase in intracellular HSP content is critical for cell survival and proteostasis under stress.
Mitochondrial Dysfunction in the Pathophysiology of Alzheimer’s Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Mitochondria are the major source of cellular ROS and subsequent stress signaling that induces cellular senescence and apoptosis]. One of the major consequences of increased ROS and altered cellular redox state is the oxidation of thiol groups in cysteine residues in relevant proteins [100]. Mitochondrial ATM kinase is one of the key modulators of the cellular stress response [101–105]. ATM kinase, which is partly located at the mitochondria, is activated upon mitochondrial uncoupling [106] and while its mitochondrial substrates are not known, loss of ATM in genetically engineered mouse models leads to mitochondrial dysfunction. ATM signaling is reduced in the neurons in vulnerable regions of the AD brain [107].
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
ER stress, also named unfolded protein response (UPR), is a cellular stress response related to the ER, which is induced by an accumulation of misfolded proteins in the ER lumen. The ER stress/UPR diminishes protein translation, degrades misfolded proteins, and produces gchaper-ones involved in protein folding in order to restore normal ER function. If this is not achieved, or the disruption is prolonged, the ER stress/UPR shifts toward promoting apoptosis.
Apelin-13 alleviates contrast-induced acute kidney injury by inhibiting endoplasmic reticulum stress
Published in Renal Failure, 2023
Qian Liu, Shao-Bin Duan, Lin Wang, Xiao-Qin Luo, Hong-Shen Wang, Ying-Hao Deng, Xi Wu, Ting Wu, Ping Yan and, Yi-Xin Kang
Previously, direct cytotoxicity associated with CM-induced apoptosis, the overproduction of reactive oxygen species (ROS) and renal hemodynamics were the potential pathogenic mechanisms of CI-AKI [8]. The use of drugs targeting apoptosis and oxidative stress regulation may be an effective therapeutic strategy [1,8]. Numerous studies have indicated that apoptosis is related to endoplasmic reticulum (ER) stress, which is a cellular stress response to the accumulation of unfolded or misfolded proteins in the ER lumen [9,10]. ER stress is thought to be an essential pathological process leading to tubular cell injury in AKI, the progression of chronic kidney disease (CKD) and the transition of AKI to CKD [9,11]. Recently, the involvement of ROS-mediated ER stress has been found in contrast-induced renal tubular cell apoptosis [12]. Therefore, the amelioration of ER stress is critical for the attenuation of CI-AKI.
Reconciling two opposing effects of radiation therapy: stimulation of cancer cell invasion and activation of anti-cancer immunity
Published in International Journal of Radiation Biology, 2023
Radiation can induce the secretion of a plethora of chemokines that attract effector T cells. This occurs as part of the cellular stress response that is most commonly regulated by NFκB (Liu et al. 2017). Matsumura S et al. showed that radiation induces the release of CXCL16 by breast cancer cells and this was sufficient to attract effector T cells leading to tumor regression (Matsumura et al. 2008). Harlin et al. found that the presence of effector T cells correlated with the expression of several well-established lymphocyte chemokines including CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10 (Harlin et al. 2009). The presence of the corresponding chemokine receptors was validated on CD8+ effector T cells. Using transwell migration assays, the authors confirmed the ability of each of these chemokines to promote migration of CD8+ effector cells in vitro.
Study on the mechanism of treating COVID-19 with Shenqi Wan based on network pharmacology
Published in Drug Development and Industrial Pharmacy, 2021
Xian-wen YE, Ya-ling Deng, Xia Zhang, Min-min Liu, Ying Liu, Ya-ting Xie, Quan Wan, Min Huang, Tao Zhang, Jia-he Xi, Jin-lian Zhang
PPI enrichment analysis was carried out using the following databases: BioGrid, InWeb-IM, and OmniPath used the MCODE algorithm to identify tightly connected network nodes. The MCODE network determined by the common target is shown in Figure 5. KEGG pathway and GO biological function enrichment analysis were applied to each MCODE node, and the three items with the highest score were calculated according to the p value. As can be seen from Figure 5, the clustering of common targets can be divided into two categories: in the first category (red), GO and KEGG pathway are the response of reactive oxygen species to inorganic substances, the response of cells to organic nitrogen compounds, the AGE-RAGE signaling pathway in diabetic complications, and toxoplasmosis, Hepatitis C. In the second category (blue), the stress response to lipopolysaccharide, the response to bacterial molecules, response to molecule of bacterial origin, second messenger mediated signaling, Toll-like receptor signaling, legionellosis, and RIG-I-like receptor signaling pathway. From the above results, the common targets are mainly involved in cellular stress response and receptor signal pathway.