Artykuły w czasopismach: „ER stress”

1

Jaenicke, Lothar. "ER-Stress". Chemie in unserer Zeit 40, nr 3 (czerwiec 2006): 161. http://dx.doi.org/10.1002/ciuz.200690036.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

2

Zito, Ester. "Targeting ER stress/ER stress response in myopathies". Redox Biology 26 (wrzesień 2019): 101232. http://dx.doi.org/10.1016/j.redox.2019.101232.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

3

Kumar, Vaishali, i Shuvadeep Maity. "ER Stress-Sensor Proteins and ER-Mitochondrial Crosstalk—Signaling Beyond (ER) Stress Response". Biomolecules 11, nr 2 (28.01.2021): 173. http://dx.doi.org/10.3390/biom11020173.

Pełny tekst źródła

Streszczenie:

Recent studies undoubtedly show the importance of inter organellar connections to maintain cellular homeostasis. In normal physiological conditions or in the presence of cellular and environmental stress, each organelle responds alone or in coordination to maintain cellular function. The Endoplasmic reticulum (ER) and mitochondria are two important organelles with very specialized structural and functional properties. These two organelles are physically connected through very specialized proteins in the region called the mitochondria-associated ER membrane (MAM). The molecular foundation of this relationship is complex and involves not only ion homeostasis through the shuttling of calcium but also many structural and apoptotic proteins. IRE1alpha and PERK are known for their canonical function as an ER stress sensor controlling unfolded protein response during ER stress. The presence of these transmembrane proteins at the MAM indicates its potential involvement in other biological functions beyond ER stress signaling. Many recent studies have now focused on the non-canonical function of these sensors. In this review, we will focus on ER mitochondrial interdependence with special emphasis on the non-canonical role of ER stress sensors beyond ER stress.

Style APA, Harvard, Vancouver, ISO itp.

4

Kawaguchi, S., i D. T. W. Ng. "Sensing ER Stress". Science 333, nr 6051 (29.09.2011): 1830–31. http://dx.doi.org/10.1126/science.1212840.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

5

Gough, N. R. "Neuronal ER Stress". Science Signaling 3, nr 152 (14.12.2010): ec378-ec378. http://dx.doi.org/10.1126/scisignal.3152ec378.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

6

Vincenz, Lisa, i F. Ulrich Hartl. "Sugarcoating ER Stress". Cell 156, nr 6 (marzec 2014): 1125–27. http://dx.doi.org/10.1016/j.cell.2014.02.035.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

7

Mateus, Duarte, Elettra Sara Marini, Cinzia Progida i Oddmund Bakke. "Rab7a modulates ER stress and ER morphology". Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1865, nr 5 (maj 2018): 781–93. http://dx.doi.org/10.1016/j.bbamcr.2018.02.011.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

8

Gorman, Adrienne M., Sandra J. M. Healy, Richard Jäger i Afshin Samali. "Stress management at the ER: Regulators of ER stress-induced apoptosis". Pharmacology & Therapeutics 134, nr 3 (czerwiec 2012): 306–16. http://dx.doi.org/10.1016/j.pharmthera.2012.02.003.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

9

Begum, Gulnaz, Lloyd Harvey, C. Edward Dixon i Dandan Sun. "ER Stress and Effects of DHA as an ER Stress Inhibitor". Translational Stroke Research 4, nr 6 (20.08.2013): 635–42. http://dx.doi.org/10.1007/s12975-013-0282-1.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

10

Lee, Amy S., i Linda M. Hendershot. "ER stress and cancer". Cancer Biology & Therapy 5, nr 7 (lipiec 2006): 721–22. http://dx.doi.org/10.4161/cbt.5.7.3120.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

11

Lee, W., W. Yoo i H. Chae. "ER Stress and Autophagy". Current Molecular Medicine 15, nr 8 (6.10.2015): 735–45. http://dx.doi.org/10.2174/1566524015666150921105453.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

12

Koo, Seung-Hoi. "Obesity and ER Stress". Korean Journal of Obesity 20, nr 2 (2011): 45. http://dx.doi.org/10.7570/kjo.2011.20.2.45.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

13

Shi, Qi, i Xiao-Ping Dong. "CtmPrP and ER stress". Prion 5, nr 3 (lipiec 2011): 123–25. http://dx.doi.org/10.4161/pri.5.3.16327.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

14

Zlotorynski, Eytan. "DR5 unfolds ER stress". Nature Reviews Molecular Cell Biology 15, nr 8 (16.07.2014): 499. http://dx.doi.org/10.1038/nrm3843.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

15

Yoshida, Hiderou. "ER stress and diseases". FEBS Journal 274, nr 3 (8.01.2007): 630–58. http://dx.doi.org/10.1111/j.1742-4658.2007.05639.x.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

16

LeBrasseur, Nicole. "ER stress shapes muscle". Journal of Cell Biology 169, nr 4 (16.05.2005): 548. http://dx.doi.org/10.1083/jcb1694iti2.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

17

Riddihough, G. "Stress Testing the ER". Science 326, nr 5958 (3.12.2009): 1323. http://dx.doi.org/10.1126/science.326.5958.1323-c.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

18

Ray, B. "STKE: Tolerating ER Stress". Science 306, nr 5698 (5.11.2004): 945c. http://dx.doi.org/10.1126/science.306.5698.945c.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

19

Binet, François, i Przemyslaw Sapieha. "ER Stress and Angiogenesis". Cell Metabolism 22, nr 4 (październik 2015): 560–75. http://dx.doi.org/10.1016/j.cmet.2015.07.010.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

20

Strzyz, Paulina. "ER stress boosts respiration". Nature Reviews Molecular Cell Biology 20, nr 8 (3.05.2019): 453. http://dx.doi.org/10.1038/s41580-019-0139-x.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

21

Collison, Joanna. "ER stress causes osteoclastogenesis". Nature Reviews Rheumatology 14, nr 4 (15.02.2018): 184. http://dx.doi.org/10.1038/nrrheum.2018.24.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

22

Hara, Takashi, i Fumihiko Urano. "ER stress and β cell death — therapeutic approach to combat ER stress". Folia Pharmacologica Japonica 144, nr 2 (2014): 53–58. http://dx.doi.org/10.1254/fpj.144.53.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

23

Miglioranza Scavuzzi, Bruna, i Joseph Holoshitz. "Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases". Antioxidants 11, nr 7 (29.06.2022): 1306. http://dx.doi.org/10.3390/antiox11071306.

Pełny tekst źródła

Streszczenie:

Background: The endoplasmic reticulum (ER) is a multi-functional organelle responsible for cellular homeostasis, protein synthesis, folding and secretion. It has been increasingly recognized that the loss of ER homeostasis plays a central role in the development of autoimmune inflammatory disorders, such as rheumatic diseases. Purpose/Main contents: Here, we review current knowledge of the contribution of ER stress to the pathogenesis of rheumatic diseases, with a focus on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We also review the interplay between protein folding and formation of reactive oxygen species (ROS), where ER stress induces oxidative stress (OS), which further aggravates the accumulation of misfolded proteins and oxidation, in a vicious cycle. Intervention studies targeting ER stress and oxidative stress in the context of rheumatic diseases are also reviewed. Conclusions: Loss of ER homeostasis is a significant factor in the pathogeneses of RA and SLE. Targeting ER stress, unfolded protein response (UPR) pathways and oxidative stress in these diseases both in vitro and in animal models have shown promising results and deserve further investigation.

Style APA, Harvard, Vancouver, ISO itp.

24

Xiao, Ting, Xiuci Liang, Hailan Liu, Feng Zhang, Wen Meng i Fang Hu. "Mitochondrial stress protein HSP60 regulates ER stress-induced hepatic lipogenesis". Journal of Molecular Endocrinology 64, nr 2 (luty 2020): 67–75. http://dx.doi.org/10.1530/jme-19-0207.

Pełny tekst źródła

Streszczenie:

Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are associated with hepatic steatosis and insulin resistance. Molecular mechanisms underlying ER stress and/or mitochondrial dysfunction that cause metabolic disorders and hepatic steatosis remain to be fully understood. Here, we found that a high fat diet (HFD) or chemically induced ER stress can stimulate mitochondrial stress protein HSP60 expression, impair mitochondrial respiration, and decrease mitochondrial membrane potential in mouse hepatocytes. HSP60 overexpression promotes ER stress and hepatic lipogenic protein expression and impairs insulin signaling in mouse hepatocytes. Mechanistically, HSP60 regulates ER stress-induced hepatic lipogenesis via the mTORC1-SREBP1 signaling pathway. These results suggest that HSP60 is an important ER and mitochondrial stress cross-talking protein and may control ER stress-induced hepatic lipogenesis and insulin resistance.

Style APA, Harvard, Vancouver, ISO itp.

25

YOSHIUCHI, Kazutomi, Hideaki KANETO, Taka-aki MATSUOKA, Ryuichi KASAMI, Kenji KOHNO, Takao IWAWAKI, Yoshihisa NAKATANI, Yoshimitsu YAMASAKI, Iichiro SHIMOMURA i Munehide MATSUHISA. "Pioglitazone Reduces ER Stress in the Liver: Direct Monitoring of in vivo ER Stress Using ER Stress-activated Indicator Transgenic Mice". Endocrine Journal 56, nr 9 (2009): 1103–11. http://dx.doi.org/10.1507/endocrj.k09e-140.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

26

Piña, Francisco Javier, Tinya Fleming, Kit Pogliano i Maho Niwa. "Reticulons Regulate the ER Inheritance Block during ER Stress". Developmental Cell 37, nr 3 (maj 2016): 279–88. http://dx.doi.org/10.1016/j.devcel.2016.03.025.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

27

Steenberg, Dorte, i Dorte Steenberg. "Stress-et fælles ansvar". Tidsskrift for Arbejdsliv 9, nr 2 (1.06.2007): 86. http://dx.doi.org/10.7146/tfa.v9i2.108613.

Pełny tekst źródła

Streszczenie:

S tress er et samfundsmæssigt problem, og det er et anliggende for arbejdspladsen. Men først og fremmest er der for det menneske, der rammes, tale om en alvorlig situation, der kan betyde sygdom og i værste fald få livsvarige konsekvenser. Sat på spidsen kan man sige, at der er tale om et forbrug af mennesker på arbejdsmarkedet og et spild af mennesker, der er helt uacceptabel. Med andre ord: der må gøres noget.

Style APA, Harvard, Vancouver, ISO itp.

28

Ong, Gideon, i Susan E. Logue. "Unfolding the Interactions between Endoplasmic Reticulum Stress and Oxidative Stress". Antioxidants 12, nr 5 (22.04.2023): 981. http://dx.doi.org/10.3390/antiox12050981.

Pełny tekst źródła

Streszczenie:

Oxidative stress is caused by an imbalance in cellular redox state due to the accumulation of reactive oxygen species (ROS). While homeostatic levels of ROS are important for cell physiology and signaling, excess ROS can induce a variety of negative effects ranging from damage to biological macromolecules to cell death. Additionally, oxidative stress can disrupt the function of redox-sensitive organelles including the mitochondria and endoplasmic reticulum (ER). In the case of the ER, the accumulation of misfolded proteins can arise due to oxidative stress, leading to the onset of ER stress. To combat ER stress, cells initiate a highly conserved stress response called the unfolded protein response (UPR). While UPR signaling, within the context of resolving ER stress, is well characterised, how UPR mediators respond to and influence oxidative stress is less defined. In this review, we evaluate the interplay between oxidative stress, ER stress and UPR signaling networks. Specifically, we assess how UPR signaling mediators can influence antioxidant responses.

Style APA, Harvard, Vancouver, ISO itp.

29

Ishiwata-Kimata, Yuki, Giang Quynh Le i Yukio Kimata. "Stress-sensing and regulatory mechanism of the endoplasmic-stress sensors Ire1 and PERK". Endoplasmic Reticulum Stress in Diseases 5, nr 1 (1.10.2018): 1–10. http://dx.doi.org/10.1515/ersc-2018-0001.

Pełny tekst źródła

Streszczenie:

Abstract Ire1 and its family protein PERK are endoplasmic reticulum (ER)-stress sensors that initiate cellular responses against ER accumulation of unfolded proteins. As reviewed in this article, many publications describe molecular mechanisms by which yeast Ire1 senses ER conditions and gets regulated. We also cover recent studies which reveal that mammalian Ire1 (IRE1α) and PERK are controlled in a similar but not exactly the same manner. ER-located molecular chaperone BiP captures these ER-stress sensors and suppresses their activity. Intriguingly, Ire1 is associated with BiP not as a chaperone substrate, but as a unique ligand. Unfolded proteins accumulated in the ER promote dissociation of the Ire1-BiP complex. Moreover, Ire1 is directly bound with unfolded proteins, leading to its cluster formation and potent activation. PERK also captures unfolded proteins and then forms self-oligomers. Meanwhile, membrane-lipid aberrancy is likely to activate these ER-stress sensors independently of ER accumulation of unfolded proteins. In addition, there exist a number of reports that touch on other factors that control activity of these ER-stress sensors. Such a multiplicity of regulatory mechanisms for these ER-stress sensors is likely to contribute to fine tuning of their activity.

Style APA, Harvard, Vancouver, ISO itp.

30

Wallington-Beddoe, Craig T., i Stuart M. Pitson. "Enhancing ER stress in myeloma". Aging 9, nr 7 (30.07.2017): 1645–46. http://dx.doi.org/10.18632/aging.101273.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

31

Wrighton, Katharine H. "Inactivating PTP1B upon ER stress". Nature Reviews Molecular Cell Biology 13, nr 2 (5.01.2012): 62–63. http://dx.doi.org/10.1038/nrm3269.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

32

Crunkhorn, Sarah. "ER stress modulator reverses diabetes". Nature Reviews Drug Discovery 14, nr 8 (31.07.2015): 528. http://dx.doi.org/10.1038/nrd4702.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

33

Hurtley, Stella M. "ER regulates stress granule fission". Science 367, nr 6477 (30.01.2020): 522.14–524. http://dx.doi.org/10.1126/science.367.6477.522-n.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

34

Lindholm, D., H. Wootz i L. Korhonen. "ER stress and neurodegenerative diseases". Cell Death & Differentiation 13, nr 3 (6.01.2006): 385–92. http://dx.doi.org/10.1038/sj.cdd.4401778.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

35

TAKAHASHI, Ryosuke. "Neurodegeneration caused by ER stress?" Folia Pharmacologica Japonica 124, nr 6 (2004): 375–82. http://dx.doi.org/10.1254/fpj.124.375.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

36

VanHook, Annalisa M. "ER-phagy to alleviate stress". Science Signaling 11, nr 516 (6.02.2018): eaat1772. http://dx.doi.org/10.1126/scisignal.aat1772.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

37

Wang, Xiaoli, Colins O. Eno, Brian J. Altman, Yanglong Zhu, Guoping Zhao, Kristen E. Olberding, Jeffrey C. Rathmell i Chi Li. "ER stress modulates cellular metabolism". Biochemical Journal 435, nr 1 (15.03.2011): 285–96. http://dx.doi.org/10.1042/bj20101864.

Pełny tekst źródła

Streszczenie:

Changes in metabolic processes play a critical role in the survival or death of cells subjected to various stresses. In the present study, we have investigated the effects of ER (endoplasmic reticulum) stress on cellular metabolism. A major difficulty in studying metabolic responses to ER stress is that ER stress normally leads to apoptosis and metabolic changes observed in dying cells may be misleading. Therefore we have used IL-3 (interleukin 3)-dependent Bak−/−Bax−/− haemopoietic cells which do not die in the presence of the ER-stress-inducing drug tunicamycin. Tunicamycin-treated Bak−/−Bax−/− cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis. In these cells, we used NMR-based SIRM (stable isotope-resolved metabolomics) to determine the metabolic effects of tunicamycin. Glucose was found to be the major carbon source for energy production and anabolic metabolism. Following tunicamycin exposure, glucose uptake and lactate production are greatly reduced. Decreased 13C labelling in several cellular metabolites suggests that mitochondrial function in cells undergoing ER stress is compromised. Consistent with this, mitochondrial membrane potential, oxygen consumption and cellular ATP levels are much lower compared with untreated cells. Importantly, the effects of tunicamycin on cellular metabolic processes may be related to a reduction in cell-surface GLUT1 (glucose transporter 1) levels which, in turn, may reflect decreased Akt signalling. These results suggest that ER stress exerts profound effects on several central metabolic processes which may help to explain cell death arising from ER stress in normal cells.

Style APA, Harvard, Vancouver, ISO itp.

38

Minamino, Tetsuo, i Masafumi Kitakaze. "ER stress in cardiovascular disease". Journal of Molecular and Cellular Cardiology 48, nr 6 (czerwiec 2010): 1105–10. http://dx.doi.org/10.1016/j.yjmcc.2009.10.026.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

39

Haspel, Jeffrey. "Surf’s up for ER stress". Science Translational Medicine 9, nr 396 (28.06.2017): eaan6728. http://dx.doi.org/10.1126/scitranslmed.aan6728.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

40

van der Harg, Judith, Anna Nolle, Susanne LaFleur, Jeroen Hoozemans i Wiep Scheper. "Metabolic stress and ER proteostasis". Mitochondrion 24 (wrzesień 2015): S5—S6. http://dx.doi.org/10.1016/j.mito.2015.07.022.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

41

Ogen-Shtern, Navit, Tamuz Ben David i Gerardo Z. Lederkremer. "Protein aggregation and ER stress". Brain Research 1648 (październik 2016): 658–66. http://dx.doi.org/10.1016/j.brainres.2016.03.044.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

42

Bird, Lucy. "ER stress induces systemic inflammation". Nature Reviews Immunology 6, nr 3 (marzec 2006): 170. http://dx.doi.org/10.1038/nri1819.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

43

Leavy, Olive. "Mismanaged ER stress and inflammation". Nature Reviews Immunology 8, nr 11 (listopad 2008): 824. http://dx.doi.org/10.1038/nri2435.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

44

Jaurez, M., A. Grenon-Girard, J. Tardif i N. Bousette. "Cardiac Lipotoxicity Causes Er Stress". Canadian Journal of Cardiology 29, nr 10 (październik 2013): S118. http://dx.doi.org/10.1016/j.cjca.2013.07.160.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

45

Zhou, Yan, Dharmani Devi Murugan, Haroon Khan, Yu Huang i Wai San Cheang. "Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases". Antioxidants 10, nr 8 (22.07.2021): 1167. http://dx.doi.org/10.3390/antiox10081167.

Pełny tekst źródła

Streszczenie:

In different pathological states that cause endoplasmic reticulum (ER) calcium depletion, altered glycosylation, nutrient deprivation, oxidative stress, DNA damage or energy perturbation/fluctuations, the protein folding process is disrupted and the ER becomes stressed. Studies in the past decade have demonstrated that ER stress is closely associated with pathogenesis of obesity, insulin resistance and type 2 diabetes. Excess nutrients and inflammatory cytokines associated with metabolic diseases can trigger or worsen ER stress. ER stress plays a critical role in the induction of endothelial dysfunction and atherosclerosis. Signaling pathways including AMP-activated protein kinase and peroxisome proliferator-activated receptor have been identified to regulate ER stress, whilst ER stress contributes to the imbalanced production between nitric oxide (NO) and reactive oxygen species (ROS) causing oxidative stress. Several drugs or herbs have been proved to protect against cardiovascular diseases (CVD) through inhibition of ER stress and oxidative stress. The present article reviews the involvement of ER stress and oxidative stress in cardiovascular dysfunction and the potential therapeutic implications.

Style APA, Harvard, Vancouver, ISO itp.

46

Booth, Laurence, Jane L. Roberts, Nichola Cruickshanks, Steven Grant, Andrew Poklepovic i Paul Dent. "Regulation of OSU-03012 Toxicity by ER Stress Proteins and ER Stress–Inducing Drugs". Molecular Cancer Therapeutics 13, nr 10 (7.08.2014): 2384–98. http://dx.doi.org/10.1158/1535-7163.mct-14-0172.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

47

Das, Indrajit, Chin Wen Png, Rajaraman D. Eri, Thu V. Tran, Rohan Lourie, Iulia Oancea, Denis I. Crane, Timothy H. Florin i Michael A. McGuckin. "Dexamethasone Ameliorates Intestinal Epithelial Cell Endoplasmic Reticulum (ER) Stress and ER Stress Induced Colitis". Gastroenterology 140, nr 5 (maj 2011): S—166. http://dx.doi.org/10.1016/s0016-5085(11)60673-2.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

48

Tardif, Keith D., Gulam Waris i Aleem Siddiqui. "Hepatitis C virus, ER stress, and oxidative stress". Trends in Microbiology 13, nr 4 (kwiecień 2005): 159–63. http://dx.doi.org/10.1016/j.tim.2005.02.004.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

49

Naidoo, Nirinjini. "ER and aging—Protein folding and the ER stress response". Ageing Research Reviews 8, nr 3 (lipiec 2009): 150–59. http://dx.doi.org/10.1016/j.arr.2009.03.001.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

50

Xu, Jiancheng, Qi Zhou, Wei Xu i Lu Cai. "Endoplasmic Reticulum Stress and Diabetic Cardiomyopathy". Experimental Diabetes Research 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/827971.

Pełny tekst źródła

Streszczenie:

The endoplasmic reticulum (ER) is an organelle entrusted with lipid synthesis, calcium homeostasis, protein folding, and maturation. Perturbation of ER-associated functions results in an evolutionarily conserved cell stress response, the unfolded protein response (UPR) that is also called ER stress. ER stress is aimed initially at compensating for damage but can eventually trigger cell death if ER stress is excessive or prolonged. Now the ER stress has been associated with numerous diseases. For instance, our recent studies have demonstrated the important role of ER stress in diabetes-induced cardiac cell death. It is known that apoptosis has been considered to play a critical role in diabetic cardiomyopathy. Therefore, this paper will summarize the information from the literature and our own studies to focus on the pathological role of ER stress in the development of diabetic cardiomyopathy. Improved understanding of the molecular mechanisms underlying UPR activation and ER-initiated apoptosis in diabetic cardiomyopathy will provide us with new targets for drug discovery and therapeutic intervention.

Style APA, Harvard, Vancouver, ISO itp.

Artykuły w czasopismach na temat „ER stress”

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych