Journal articles: 'Stress response pathways'

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Leiser, Scott, Christopher Choi, Ajay Bhat, and Charles Evans. "A Metabolic Stress Response." Innovation in Aging 4, Supplement_1 (December 1, 2020): 123. http://dx.doi.org/10.1093/geroni/igaa057.404.

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Abstract An organism’s ability to respond to stress is crucial for long-term survival. These stress responses are coordinated by distinct but overlapping pathways, many of which have been found to also regulate longevity in multiple organisms across species. Despite extensive effort, our understanding of these pathways and how they affect aging remains incomplete and thus is a key area of study in Geroscience. Our previous work identified flavin-containing monooxygenase-2 (fmo-2) as a key longevity-promoting gene downstream of at least three longevity promoting pathways, including the hypoxic response, the pentose phosphate pathway, and the dietary restriction pathway. Based on the commonalities of these pathways, we hypothesized that fmo-2, a classically annotated xenobiotic enzyme, might play a key endogenous role in responding to metabolic stress. Our resulting data, using metabolic profiling and further epistatic analysis, both support this hypothesis and link fmo-2’s mechanism to modifications to one-carbon metabolism (OCM), a key intermediate pathway between the nucleotide metabolism, methylation, and transsulfuration pathways. Using mathematical modeling and a novel metabolomics approach, we were able to further identify the likely mechanism of fmo-2-mediated metabolic effects, and connect them to both OCM and downstream components. We propose a model whereby nematode fmo-2 represents a class of enzymes that are able to modify large aspects of metabolism, similar to how transcription factors modify gene expression, and that fmo-2 is a key member of a conserved metabolic stress response.

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Jennings, Paul. "Stress response pathways, toxicity pathways and adverse outcome pathways." Archives of Toxicology 87, no. 1 (November 13, 2012): 13–14. http://dx.doi.org/10.1007/s00204-012-0974-4.

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Vonlaufen, Nathalie, Stefan M. Kanzok, Ronald C. Wek, and William J. Sullivan Jr. "Stress response pathways in protozoan parasites." Cellular Microbiology 10, no. 12 (December 2008): 2387–99. http://dx.doi.org/10.1111/j.1462-5822.2008.01210.x.

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Jayasinghe, Sisitha Udara, Sarah Janet Hall, Susan Jane Torres, and Anne Isabella Turner. "Stress system dysfunction revealed by integrating reactivity of stress pathways to psychological stress in lean and overweight/obese men." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 322, no. 2 (February 1, 2022): R144—R151. http://dx.doi.org/10.1152/ajpregu.00276.2021.

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Although the patterns of response within the sympathoadrenal medullary (SAM) system and hypothalamo-pituitary adrenal (HPA) axis are interesting and important in their own accord, the overall response to acute psychological stress involves reactivity of both pathways. We tested the hypothesis that consideration of the integrated response of these pathways may reveal dysregulation of the stress systems, which is not evident when considering either system alone. Age-matched lean and overweight/obese men were subjected to a Trier Social Stress Test and reactivity of the SAM system (salivary α-amylase, systolic blood pressure, diastolic blood pressure, and heart rate) and the HPA axis (salivary cortisol) were measured. Relative reactivity of SAM system and HPA axis was calculated as the ratio between the measures from each pathway. Although analysis of reactivity of individual stress pathways showed no evidence of dysfunction in overweight/obese compared with lean men, analysis of HPA/SAM reactivity revealed significantly lower cortisol over systolic blood pressure (CoSBP) and cortisol over diastolic blood pressure (CoDBP) reactivity in overweight/obese compared with lean men. Other measures of HPA/SAM reactivity and all measures of SAM/HPA reactivity were unaltered in overweight/obese compared with lean men. These findings suggest that the cortisol response per unit of blood pressure response is blunted in men with elevated adiposity. Furthermore, these findings support a notion of a coordinated overall approach to activation of the stress pathways with the degree of activation in one pathway being related to the degree of activation in the other.

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Romero, L. M., and B. M. G. Gormally. "How Truly Conserved Is the “Well-Conserved” Vertebrate Stress Response?" Integrative and Comparative Biology 59, no. 2 (April 22, 2019): 273–81. http://dx.doi.org/10.1093/icb/icz011.

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Abstract The vertebrate stress response is considered to be a highly conserved suite of responses that are evolved to help animals survive noxious environmental stimuli. The two major pathways of the stress response include the catecholamine release that is part of the autonomic nervous system and comprises the immediate fight-or-flight response, and the slower release of corticosteroids from the hypothalamic–pituitary–adrenal axis that help orchestrate longer-term responses. These two pathways are present in every vertebrate yet examined, and the anatomical and physiological architecture underlying these pathways are consistent. Despite these structural similarities, however, recent data indicate substantial temporal and species variation in the actual regulation of these pathways. For example, activation of both pathways varies seasonally in some species but not others, and responses of both pathways can be extensively modulated by an individual’s previous experience. Consequently, even though the anatomy of the stress response is highly conserved, the activation and functional output is not highly conserved. Given this variation, it is perhaps not surprising that it is proving difficult to correlate individual stress responses with differences in fitness outcomes. This review summarizes the challenge of making broad generalized assumptions about fitness consequences of the stress response given the functional variation we observe.

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Araki, Eiichi, Tatsuya Kondo, and Hirofumi Kai. "Cellular stress response pathways and diabetes mellitus." Diabetology International 6, no. 4 (August 18, 2015): 239–42. http://dx.doi.org/10.1007/s13340-015-0229-8.

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Tew, Kenneth D. "Hematopoiesis, S-Glutathionylation and Stress Response Pathways." Free Radical Biology and Medicine 96 (July 2016): S10. http://dx.doi.org/10.1016/j.freeradbiomed.2016.04.051.

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Moore, James, Ivan Osinnii, Amandine Grimm, Björn Oettinghaus, Anne Eckert, Stephan Frank, and Erik C. Böttger. "Silencing of the ER and Integrative Stress Responses in the Liver of Mice with Error-Prone Translation." Cells 10, no. 11 (October 23, 2021): 2856. http://dx.doi.org/10.3390/cells10112856.

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Translational errors frequently arise during protein synthesis, producing misfolded and dysfunctional proteins. Chronic stress resulting from translation errors may be particularly relevant in tissues that must synthesize and secrete large amounts of secretory proteins. Here, we studied the proteostasis networks in the liver of mice that express the Rps2-A226Y ribosomal ambiguity (ram) mutation to increase the translation error rate across all proteins. We found that Rps2-A226Y mice lack activation of the eIF2 kinase/ATF4 pathway, the main component of the integrated stress response (ISR), as well as the IRE1 and ATF6 pathways of the ER unfolded protein response (ER-UPR). Instead, we found downregulation of chronic ER stress responses, as indicated by reduced gene expression for lipogenic pathways and acute phase proteins, possibly via upregulation of Sirtuin-1. In parallel, we observed activation of alternative proteostasis responses, including the proteasome and the formation of stress granules. Together, our results point to a concerted response to error-prone translation to alleviate ER stress in favor of activating alternative proteostasis mechanisms, most likely to avoid cell damage and apoptotic pathways, which would result from persistent activation of the ER and integrated stress responses.

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Kim, Eunjung, Jae-Young Kim, and Joo-Yong Lee. "Mathematical Modeling of p53 Pathways." International Journal of Molecular Sciences 20, no. 20 (October 18, 2019): 5179. http://dx.doi.org/10.3390/ijms20205179.

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Cells have evolved balanced systems that ensure an appropriate response to stress. The systems elicit repair responses in temporary or moderate stress but eliminate irreparable cells via apoptosis in detrimental conditions of prolonged or severe stress. The tumor suppressor p53 is a central player in these stress response systems. When activated under DNA damage stress, p53 regulates hundreds of genes that are involved in DNA repair, cell cycle, and apoptosis. Recently, increasing studies have demonstrated additional regulatory roles of p53 in metabolism and mitochondrial physiology. Due to the inherent complexity of feedback loops between p53 and its target genes, the application of mathematical modeling has emerged as a novel approach to better understand the multifaceted functions and dynamics of p53. In this review, we discuss several mathematical modeling approaches in exploring the p53 pathways.

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Doonan, Liam B., Ashlie Hartigan, Beth Okamura, and Paul F. Long. "Stress-Free Evolution: The Nrf-Coordinated Oxidative Stress Response in Early Diverging Metazoans." Integrative and Comparative Biology 59, no. 4 (May 23, 2019): 799–810. http://dx.doi.org/10.1093/icb/icz055.

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Abstract Environmental stress from ultraviolet radiation, elevated temperatures or metal toxicity can lead to reactive oxygen species in cells, leading to oxidative DNA damage, premature aging, neurodegenerative diseases, and cancer. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activates many cytoprotective proteins within the nucleus to maintain homeostasis during oxidative stress. In vertebrates, Nrf2 levels are regulated by the Kelch-family protein Keap1 (Kelch-like ECH-associated protein 1) in the absence of stress according to a canonical redox control pathway. Little, however, is known about the redox control pathway used in early diverging metazoans. Our study examines the presence of known oxidative stress regulatory elements within non-bilaterian metazoans including free living and parasitic cnidarians, ctenophores, placozoans, and sponges. Cnidarians, with their pivotal position as the sister phylum to bilaterians, play an important role in understanding the evolutionary history of response to oxidative stress. Through comparative genomic and transcriptomic analysis our results show that Nrf homologs evolved early in metazoans, whereas Keap1 appeared later in the last common ancestor of cnidarians and bilaterians. However, key Nrf–Keap1 interacting domains are not conserved within the cnidarian lineage, suggesting this important pathway evolved with the radiation of bilaterians. Several known downstream Nrf targets are present in cnidarians suggesting that cnidarian Nrf plays an important role in oxidative stress response even in the absence of Keap1. Comparative analyses of key oxidative stress sensing and response proteins in early diverging metazoans thus provide important insights into the molecular basis of how these lineages interact with their environment and suggest a shared evolutionary history of regulatory pathways. Exploration of these pathways may prove important for the study of cancer therapeutics and broader research in oxidative stress, senescence, and the functional responses of early diverging metazoans to environmental change.

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Kulp, Adam, and Meta J. Kuehn. "Recognition of β-Strand Motifs by RseB Is Required for σEActivity in Escherichia coli." Journal of Bacteriology 193, no. 22 (September 9, 2011): 6179–86. http://dx.doi.org/10.1128/jb.05657-11.

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Gram-negative bacteria react to misfolded proteins in the envelope through a myriad of different stress response pathways. This cohort of pathways allows the bacteria to specifically respond to different types of damage, and many of these have been discovered to have key roles in the virulence of bacterial pathogens. Misfolded outer membrane proteins (OMPs) are typically recognized by the σEpathway, a highly conserved envelope stress response pathway. We examined the features of misfolded OMPs with respect to their ability to generate envelope stress responses. We determined that the secondary structure, particularly the potential to form β strands, is critical to inducing the σEresponse in an RseB-dependent manner. The sequence of the potential β-strand motif modulates the strength of the σEresponse generated by the constructs. By understanding the details of how such stress response pathways are activated, we can gain a greater understanding of how bacteria survive in harsh environments.

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Semkova, Vesselina, Simone Haupt, Michaela Segschneider, Catherine Bell, Magnus Ingelman-Sundberg, Mohamad Hajo, Beatrice Weykopf, Pathma Muthukottiappan, Andreas Till, and Oliver Brüstle. "Dynamics of Metabolic Pathways and Stress Response Patterns during Human Neural Stem Cell Proliferation and Differentiation." Cells 11, no. 9 (April 20, 2022): 1388. http://dx.doi.org/10.3390/cells11091388.

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Understanding early nervous system stress response mechanisms is crucial for studying developmental neurotoxicity and devising neuroprotective treatments. We used hiPSC-derived long-term self-renewing neuroepithelial stem (lt-NES) cells differentiated for up to 12 weeks as an in vitro model of human neural development. Following a transcriptome analysis to identify pathway alterations, we induced acute oxidative stress (OS) using tert-butyl hydroperoxide (TBHP) and assessed cell viability at different stages of neural differentiation. We studied NRF2 activation, autophagy, and proteasomal function to explore the contribution and interplay of these pathways in the acute stress response. With increasing differentiation, lt-NES cells showed changes in the expression of metabolic pathway-associated genes with engagement of the pentose phosphate pathway after 6 weeks, this was accompanied by a decreased susceptibility to TBHP-induced stress. Microarray analysis revealed upregulation of target genes of the antioxidant response KEAP1–NRF2–ARE pathway after 6 weeks of differentiation. Pharmacological inhibition of NRF2 confirmed its vital role in the increased resistance to stress. While autophagy was upregulated alongside differentiation, it was not further increased upon oxidative stress and had no effect on stress-induced cell loss and the activation of NRF2 downstream genes. In contrast, proteasome inhibition led to the aggravation of the stress response resulting in decreased cell viability, derangement of NRF2 and KEAP1 protein levels, and lacking NRF2-pathway activation. Our data provide detailed insight into the dynamic regulation and interaction of pathways involved in modulating stress responses across defined time points of neural differentiation.

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Soo, Sonja K., Annika Traa, Paige D. Rudich, Meeta Mistry, and Jeremy M. Van Raamsdonk. "Activation of mitochondrial unfolded protein response protects against multiple exogenous stressors." Life Science Alliance 4, no. 12 (September 28, 2021): e202101182. http://dx.doi.org/10.26508/lsa.202101182.

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The mitochondrial unfolded protein response (mitoUPR) is an evolutionarily conserved pathway that responds to mitochondria insults through transcriptional changes, mediated by the transcription factor ATFS-1/ATF-5, which acts to restore mitochondrial homeostasis. In this work, we characterized the role of ATFS-1 in responding to organismal stress. We found that activation of ATFS-1 is sufficient to cause up-regulation of genes involved in multiple stress response pathways including the DAF-16–mediated stress response pathway, the cytosolic unfolded protein response, the endoplasmic reticulum unfolded protein response, the SKN-1–mediated oxidative stress response pathway, the HIF-1-mediated hypoxia response pathway, the p38-mediated innate immune response pathway, and antioxidant genes. Constitutive activation of ATFS-1 increases resistance to multiple acute exogenous stressors, whereas disruption of atfs-1 decreases stress resistance. Although ATFS-1–dependent genes are up-regulated in multiple long-lived mutants, constitutive activation of ATFS-1 decreases lifespan in wild-type animals. Overall, our work demonstrates that ATFS-1 serves a vital role in organismal survival of acute stressors through its ability to activate multiple stress response pathways but that chronic ATFS-1 activation is detrimental for longevity.

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Ku, Yee-Shan, Mariz Sintaha, Ming-Yan Cheung, and Hon-Ming Lam. "Plant Hormone Signaling Crosstalks between Biotic and Abiotic Stress Responses." International Journal of Molecular Sciences 19, no. 10 (October 17, 2018): 3206. http://dx.doi.org/10.3390/ijms19103206.

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In the natural environment, plants are often bombarded by a combination of abiotic (such as drought, salt, heat or cold) and biotic (necrotrophic and biotrophic pathogens) stresses simultaneously. It is critical to understand how the various response pathways to these stresses interact with one another within the plants, and where the points of crosstalk occur which switch the responses from one pathway to another. Calcium sensors are often regarded as the first line of response to external stimuli to trigger downstream signaling. Abscisic acid (ABA) is a major phytohormone regulating stress responses, and it interacts with the jasmonic acid (JA) and salicylic acid (SA) signaling pathways to channel resources into mitigating the effects of abiotic stresses versus defending against pathogens. The signal transduction in these pathways are often carried out via GTP-binding proteins (G-proteins) which comprise of a large group of proteins that are varied in structures and functions. Deciphering the combined actions of these different signaling pathways in plants would greatly enhance the ability of breeders to develop food crops that can thrive in deteriorating environmental conditions under climate change, and that can maintain or even increase crop yield.

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Fuess, Lauren E., Jorge H. Pinzón C, Ernesto Weil, Robert D. Grinshpon, and Laura D. Mydlarz. "Life or death: disease-tolerant coral species activate autophagy following immune challenge." Proceedings of the Royal Society B: Biological Sciences 284, no. 1856 (June 7, 2017): 20170771. http://dx.doi.org/10.1098/rspb.2017.0771.

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Global climate change has increased the number and severity of stressors affecting species, yet not all species respond equally to these stressors. Organisms may employ cellular mechanisms such as apoptosis and autophagy in responding to stressful events. These two pathways are often mutually exclusive, dictating whether a cell adapts or dies. In order to examine differences in cellular response to stress, we compared the immune response of four coral species with a range of disease susceptibility. Using RNA-seq and novel pathway analysis, we were able to identify differences in response to immune stimulation between these species. Disease-susceptible species Orbicella faveolata activated pathways associated with apoptosis. By contrast, disease-tolerant species Porites porites and Porites astreoides activated autophagic pathways. Moderately susceptible species Pseudodiploria strigosa activated a mixture of these pathways. These findings were corroborated by apoptotic caspase protein assays, which indicated increased caspase activity following immune stimulation in susceptible species. Our results indicate that in response to immune stress, disease-tolerant species activate cellular adaptive mechanisms such as autophagy, while susceptible species turn on cell death pathways. Differences in these cellular maintenance pathways may therefore influence the organismal stress response. Further study of these pathways will increase understanding of differential stress response and species survival in the face of changing environments.

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Islam, Md Zakirul, Md Mehedi Hasan Khandakar, Md Harun-ur Rashid, and Mohammad Shohel Rana Siddiki. "Stress Response Pathways in Dairy Cattle: A Brief Review." International Science Review 1, no. 1 (July 30, 2020): 49–53. http://dx.doi.org/10.47285/isr.v1i1.28.

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Stress is an external event or condition that places a strain on a biological system. The animal response to stress involves the expenditure of energy to remove or reduce the impact of stress. This increases the maintenance requirements of the animal and results in loss of production. The biological response to stress is divided into acute and chronic phases, with the acute phase lasting hours to a few days, and the chronic phase lasting several days to weeks. The acute response is driven by homeostatic regulators of the nervous and endocrine systems and the chronic phase by homeorhetic regulators of the endocrine system. Both responses involve alterations in energy balance and metabolism. The thermal environment affects all animals and therefore represents the largest single stressor in animal production. Other types of stressors include housing conditions, overcrowding, social rank, disease, and toxic compounds. "Acclimation" to stress is a phenotypic response developed by the animal to an individual stressor within the environment. Acclimation is a homeorhetic process that takes several weeks to occur and occurs via homeorhetic, not homeostatic, mechanisms. It is a phenotypic change that disappears when the stress is removed. Milk yield and reproduction are extremely sensitive to stress because of the high energy and protein demands of lactation and the complexity of the reproductive process and multiple organs that are involved. Improvements in the protection of animals against stress require improved education of producers to recognize stress and methods for estimating the degree of stress on animals.

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Papadakis, Manos A., and Christopher T. Workman. "Oxidative stress response pathways: Fission yeast as archetype." Critical Reviews in Microbiology 41, no. 4 (October 2, 2015): 520–35. http://dx.doi.org/10.3109/1040841x.2013.870968.

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Sridharan, Sriram, Rajani Varghese, Vijay Venkatraj, and Aniruddha Datta. "Hypoxia Stress Response Pathways: Modeling and Targeted Therapy." IEEE Journal of Biomedical and Health Informatics 21, no. 3 (May 2017): 875–85. http://dx.doi.org/10.1109/jbhi.2016.2559460.

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Boyle, Maureen P., Judson A. Brewer, Sherri K. Vogt, David F. Wozniak, and Louis J. Muglia. "Genetic Dissection of Stress Response Pathways In Vivo." Endocrine Research 30, no. 4 (January 2004): 859–63. http://dx.doi.org/10.1081/erc-200044120.

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Ikner, Aminah, and Kazuhiro Shiozaki. "Yeast signaling pathways in the oxidative stress response." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 569, no. 1-2 (January 2005): 13–27. http://dx.doi.org/10.1016/j.mrfmmm.2004.09.006.

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Pearce, Amanda K., and Timothy C. Humphrey. "Integrating stress-response and cell-cycle checkpoint pathways." Trends in Cell Biology 11, no. 10 (October 2001): 426–33. http://dx.doi.org/10.1016/s0962-8924(01)02119-5.

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al’Absi, Mustafa. "Stress response pathways, appetite regulation, and drug addiction." Biological Psychology 131 (January 2018): 1–4. http://dx.doi.org/10.1016/j.biopsycho.2017.11.012.

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Moulton, W. "Business failure pathways: Environmental stress and organizational response." Journal of Management 22, no. 4 (1996): 571–95. http://dx.doi.org/10.1016/s0149-2063(96)90025-2.

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Fahie, Kamau M. M., Kyriakos N. Papanicolaou, and Natasha E. Zachara. "Integration of O-GlcNAc into Stress Response Pathways." Cells 11, no. 21 (November 5, 2022): 3509. http://dx.doi.org/10.3390/cells11213509.

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The modification of nuclear, mitochondrial, and cytosolic proteins by O-linked βN-acetylglucosamine (O-GlcNAc) has emerged as a dynamic and essential post-translational modification of mammalian proteins. O-GlcNAc is cycled on and off over 5000 proteins in response to diverse stimuli impacting protein function and, in turn, epigenetics and transcription, translation and proteostasis, metabolism, cell structure, and signal transduction. Environmental and physiological injury lead to complex changes in O-GlcNAcylation that impact cell and tissue survival in models of heat shock, osmotic stress, oxidative stress, and hypoxia/reoxygenation injury, as well as ischemic reperfusion injury. Numerous mechanisms that appear to underpin O-GlcNAc-mediated survival include changes in chaperone levels, impacts on the unfolded protein response and integrated stress response, improvements in mitochondrial function, and reduced protein aggregation. Here, we discuss the points at which O-GlcNAc is integrated into the cellular stress response, focusing on the roles it plays in the cardiovascular system and in neurodegeneration.

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Lamech, Lilian T., and Cole M. Haynes. "The unpredictability of prolonged activation of stress response pathways." Journal of Cell Biology 209, no. 6 (June 22, 2015): 781–87. http://dx.doi.org/10.1083/jcb.201503107.

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In response to stress, cellular compartments activate signaling pathways that mediate transcriptional programs to promote survival and reestablish homeostasis. Manipulation of the magnitude and duration of the activation of stress responses has been proposed as a strategy to prevent or repair the damage associated with aging or degenerative diseases. However, as these pathways likely evolved to respond specifically to transient perturbations, the unpredictability of prolonged activation should be considered.

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Sharma, Rohit B., Christine Darko, and Laura C. Alonso. "Intersection of the ATF6 and XBP1 ER stress pathways in mouse islet cells." Journal of Biological Chemistry 295, no. 41 (August 11, 2020): 14164–77. http://dx.doi.org/10.1074/jbc.ra120.014173.

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Success or failure of pancreatic beta cell adaptation to ER stress is a determinant of diabetes susceptibility. The ATF6 and IRE1/XBP1 pathways are separate ER stress-response effectors important to beta cell health and function. ATF6α. and XBP1 direct overlapping transcriptional responses in some cell types. However, the signaling dynamics and interdependence of ATF6α and XBP1 in pancreatic beta cells have not been explored. To assess pathway-specific signal onset, we performed timed exposures of primary mouse islet cells to ER stressors and measured the early transcriptional response. Comparing the time course of induction of ATF6 and XBP1 targets suggested that the two pathways have similar response dynamics. The role of ATF6α in target induction was assessed by acute knockdown using islet cells from Atf6αflox/flox mice transduced with adenovirus expressing Cre recombinase. Surprisingly, given the mild impact of chronic deletion in mice, acute ATF6α knockdown markedly reduced ATF6-pathway target gene expression under both basal and stressed conditions. Intriguingly, although ATF6α knockdown did not alter Xbp1 splicing dynamics or intensity, it did reduce induction of XBP1 targets. Inhibition of Xbp1 splicing did not decrease induction of ATF6α targets. Taken together, these data suggest that the XBP1 and ATF6 pathways are simultaneously activated in islet cells in response to acute stress and that ATF6α is required for full activation of XBP1 targets, but XBP1 is not required for activation of ATF6α targets. These observations improve understanding of the ER stress transcriptional response in pancreatic islets.

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Ashcroft, Margaret, Yoichi Taya, and Karen H. Vousden. "Stress Signals Utilize Multiple Pathways To Stabilize p53." Molecular and Cellular Biology 20, no. 9 (May 1, 2000): 3224–33. http://dx.doi.org/10.1128/mcb.20.9.3224-3233.2000.

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ABSTRACT The p53 tumor suppressor is activated by many diverse stress signals through mechanisms that result in stabilization and accumulation of the p53 protein. p53 is normally degraded through the proteasome following interaction with MDM2, which both functions as a ubiquitin ligase for p53 and shuttles to the cytoplasm, where p53 degradation occurs. Stabilization of p53 in response to stress is associated with inhibition of MDM2-mediated degradation, which has been associated with phosphorylation of p53 in response to DNA damage or activation of ARF. In this study we show distinct responses, as measured by phosphorylation, transcriptional activity, and subcellular localization, of p53 stabilized by different activating signals. Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested. Our results show that multiple pathways exist to stabilize p53 in response to different forms of stress, and they may involve down-regulation of MDM2 expression or regulation of the subcellular localization of p53 or MDM2. Loss of any one of these pathways may predispose cells to malignant transformation, although reactivation of p53 might be achieved through alternative pathways that remain functional in these tumor cells.

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Vind, Anna Constance, Aitana Victoria Genzor, and Simon Bekker-Jensen. "Ribosomal stress-surveillance: three pathways is a magic number." Nucleic Acids Research 48, no. 19 (September 17, 2020): 10648–61. http://dx.doi.org/10.1093/nar/gkaa757.

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Abstract Cells rely on stress response pathways to uphold cellular homeostasis and limit the negative effects of harmful environmental stimuli. The stress- and mitogen-activated protein (MAP) kinases, p38 and JNK, are at the nexus of numerous stress responses, among these the ribotoxic stress response (RSR). Ribosomal impairment is detrimental to cell function as it disrupts protein synthesis, increase inflammatory signaling and, if unresolved, lead to cell death. In this review, we offer a general overview of the three main translation surveillance pathways; the RSR, Ribosome-associated Quality Control (RQC) and the Integrated Stress Response (ISR). We highlight recent advances made in defining activation mechanisms for these pathways and discuss their commonalities and differences. Finally, we reflect on the physiological role of the RSR and consider the therapeutic potential of targeting the sensing kinase ZAKα for treatment of ribotoxin exposure.

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MATHIAS, Shalini, Louis A. PEÑA, and Richard N. KOLESNICK. "Signal transduction of stress via ceramide." Biochemical Journal 335, no. 3 (November 1, 1998): 465–80. http://dx.doi.org/10.1042/bj3350465.

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The sphingomyelin (SM) pathway is a ubiquitous, evolutionarily conserved signalling system analogous to conventional systems such as the cAMP and phosphoinositide pathways. Ceramide, which serves as second messenger in this pathway, is generated from SM by the action of a neutral or acidic SMase, or by de novosynthesis co-ordinated through the enzyme ceramide synthase. A number of direct targets for ceramide action have now been identified, including ceramide-activated protein kinase, ceramide-activated protein phosphatase and protein kinase Cζ, which couple the SM pathway to well defined intracellular signalling cascades. The SM pathway induces differentiation, proliferation or growth arrest, depending on the cell type. Very often, however, the outcome of signalling through this pathway is apoptosis. Mammalian systems respond to diverse stresses with ceramide generation, and recent studies show that yeast manifest a form of this response. Thus ceramide signalling is an older stress response system than the caspase/apoptotic death pathway, and hence these two pathways must have become linked later in evolution. Signalling of the stress response through ceramide appears to play a role in the development of human diseases, including ischaemia/reperfusion injury, insulin resistance and diabetes, atherogenesis, septic shock and ovarian failure. Further, ceramide signalling mediates the therapeutic effects of chemotherapy and radiation in some cells. An understanding of the mechanisms by which ceramide regulates physiological and pathological events in specific cells may provide new targets for pharmacological intervention.

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Zhou, Yunzhuan, Fuxiang Xu, Yanan Shao, and Junna He. "Regulatory Mechanisms of Heat Stress Response and Thermomorphogenesis in Plants." Plants 11, no. 24 (December 7, 2022): 3410. http://dx.doi.org/10.3390/plants11243410.

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As worldwide warming intensifies, the average temperature of the earth continues to increase. Temperature is a key factor for the growth and development of all organisms and governs the distribution and seasonal behavior of plants. High temperatures lead to various biochemical, physiological, and morphological changes in plants and threaten plant productivity. As sessile organisms, plants are subjected to various hostile environmental factors and forced to change their cellular state and morphological architecture to successfully deal with the damage they suffer. Therefore, plants have evolved multiple strategies to cope with an abnormal rise in temperature. There are two main mechanisms by which plants respond to elevated environmental temperatures. One is the heat stress response, which is activated under extremely high temperatures; the other is the thermomorphogenesis response, which is activated under moderately elevated temperatures, below the heat-stress range. In this review, we summarize recent progress in the study of these two important heat-responsive molecular regulatory pathways mediated, respectively, by the Heat Shock Transcription Factor (HSF)–Heat Shock Protein (HSP) pathway and PHYTOCHROME INTER-ACTING FACTOR 4 (PIF4) pathways in plants and elucidate the regulatory mechanisms of the genes involved in these pathways to provide comprehensive data for researchers studying the heat response. We also discuss future perspectives in this field.

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Wang, Jia, Li Song, Xue Gong, Jinfan Xu, and Minhui Li. "Functions of Jasmonic Acid in Plant Regulation and Response to Abiotic Stress." International Journal of Molecular Sciences 21, no. 4 (February 20, 2020): 1446. http://dx.doi.org/10.3390/ijms21041446.

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Jasmonic acid (JA) is an endogenous growth-regulating substance, initially identified as a stress-related hormone in higher plants. Similarly, the exogenous application of JA also has a regulatory effect on plants. Abiotic stress often causes large-scale plant damage. In this review, we focus on the JA signaling pathways in response to abiotic stresses, including cold, drought, salinity, heavy metals, and light. On the other hand, JA does not play an independent regulatory role, but works in a complex signal network with other phytohormone signaling pathways. In this review, we will discuss transcription factors and genes involved in the regulation of the JA signaling pathway in response to abiotic stress. In this process, the JAZ-MYC module plays a central role in the JA signaling pathway through integration of regulatory transcription factors and related genes. Simultaneously, JA has synergistic and antagonistic effects with abscisic acid (ABA), ethylene (ET), salicylic acid (SA), and other plant hormones in the process of resisting environmental stress.

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Bonilla, Carla Y. "Generally Stressed Out Bacteria: Environmental Stress Response Mechanisms in Gram-Positive Bacteria." Integrative and Comparative Biology 60, no. 1 (February 11, 2020): 126–33. http://dx.doi.org/10.1093/icb/icaa002.

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Abstract The ability to monitor the environment for toxic chemical and physical disturbances is essential for bacteria that live in dynamic environments. The fundamental sensing mechanisms and physiological responses that allow bacteria to thrive are conserved even if the molecular components of these pathways are not. The bacterial general stress response (GSR) represents a conceptual model for how one pathway integrates a wide range of environmental signals, and how a generalized system with broad molecular responses is coordinated to promote survival likely through complementary pathways. Environmental stress signals such as heat, osmotic stress, and pH changes are received by sensor proteins that through a signaling cascade activate the sigma factor, SigB, to regulate over 200 genes. Additionally, the GSR plays an important role in stress priming that increases bacterial fitness to unrelated subsequent stressors such as oxidative compounds. While the GSR response is implicated during oxidative stress, the reason for its activation remains unknown and suggests crosstalk between environmental and oxidative stress sensors and responses to coordinate antioxidant functions. Systems levels studies of cellular responses such as transcriptomes, proteomes, and metabolomes of stressed bacteria and single-cell analysis could shed light into the regulated functions that protect, remediate, and minimize damage during dynamic environments. This perspective will focus on fundamental stress sensing mechanisms and responses in Gram-positive bacterial species to illustrate their commonalities at the molecular and physiological levels; summarize exciting directions; and highlight how system-level approaches can help us understand bacterial physiology.

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Herr, Ingrid, and Klaus-Michael Debatin. "Cellular stress response and apoptosis in cancer therapy." Blood 98, no. 9 (November 1, 2001): 2603–14. http://dx.doi.org/10.1182/blood.v98.9.2603.

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Abstract Anticancer treatment using cytotoxic drugs is considered to mediate cell death by activating key elements of the apoptosis program and the cellular stress response. While proteolytic enzymes (caspases) serve as main effectors of apoptosis, the mechanisms involved in activation of the caspase system are less clear. Two distinct pathways upstream of the caspase cascade have been identified. Death receptors, eg, CD95 (APO-1/Fas), trigger caspase-8, and mitochondria release apoptogenic factors (cytochrome c, Apaf-1, AIF), leading to the activation of caspase-9. The stressed endoplasmic reticulum (ER) contributes to apoptosis by the unfolded protein response pathway, which induces ER chaperones, and by the ER overload response pathway, which produces cytokines via nuclear factor-κB. Multiple other stress-inducible molecules, such as p53, JNK, AP-1, NF-κB, PKC/MAPK/ERK, and members of the sphingomyelin pathway have a profound influence on apoptosis. Understanding the complex interaction between different cellular programs provides insights into sensitivity or resistance of tumor cells and identifies molecular targets for rational therapeutic intervention strategies.

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Lyu, Keliang, Kailun Shi, Chengkun Liu, Zhiwen Lyu, Dongwu Liu, and Xue Wang. "The Sensitive Genes in Response to Various Metal Ion Stresses in the Yeast Saccharomyces cerevisiae." Protein & Peptide Letters 29, no. 3 (March 2022): 231–41. http://dx.doi.org/10.2174/0929866529666220126102348.

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Abstract: Yeast Saccharomyces cerevisiae is a good eukaryotic model for studying the molecular mechanism of toxic metal ion stress. Numerous studies have been performed on the signal transduction induced by toxic metal ion stress. The physiological process of eukaryotic cells has been studied and various stress factors have been elucidated by constructing gene deletion library. Until now, the sensitivity and tolerance mechanism of yeast under metal ion stress have been widely studied. The sensitive genes induced by metal ion stress will provide a key foundation for studying the gene function of eukaryotic organisms. In addition, the functions of genes in response to metal ion stress mainly participate in regulating ion homeostasis, high glycerin pathway, vacuole protein separation pathway, cell wall integrity pathway, and cell autophagy. However, the interaction of these signal pathways and the detailed response mechanism need to be further studied in future. In addition, the technique of genomics and proteomics will be helpful for studying the detailed molecular mechanism induced by toxic metal ion stress. Thus, the sensitive genes related to various signal pathways under toxic metal ion stress will be reviewed in the yeast S. cerevisiae.

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Zeybek, Naciye Dilara, Eylem Baysal, Ozlem Bozdemir, and Esra Buber. "Hippo Signaling: A Stress Response Pathway in Stem Cells." Current Stem Cell Research & Therapy 16, no. 7 (September 3, 2021): 824–39. http://dx.doi.org/10.2174/1574888x16666210712100002.

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The Hippo pathway, with its core components and the downstream transcriptional coactivators, controls the self-renewable capacity and stemness features of stem cells and serves as a stress response pathway by regulating proliferation, differentiation and apoptosis. The Hippo pathway interaction with other signaling pathways plays an important role in response to various stress stimuli arising from energy metabolism, hypoxia, reactive oxygen species, and mechanical forces. Depending on the energy levels, the Hippo pathway is regulated by AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR), which in turn determines stem cell proliferation (cell survival and growth) and differentiation. Oxidative stress-driven by ROS production also affects the Hippo pathway with transcriptional changes through MST/YAP/FoxO pathway and leads to the activation of pro-apoptotic genes and eventually cell death. HIF1alpha/YAP signaling is critical for the long-term maintenance of mesenchymal stem cells (MSCs) under hypoxia. In this review, we present an overview of stem cell response to stress, including mechanical, hypoxia, metabolic and oxidative stress through the modulation of the Hippo pathway. The biological effects such as autophagy, apoptosis and senescence were discussed in the context of the Hippo pathway in stem cells.

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Miao, Yaodong, Rui Chen, Zeyu Zhang, Yaoyuan Liu, Fengwen Yang, and Junhua Zhang. "Network Pharmacology Analysis of Xuanfei Baidu Granule in the Treatment of Intestinal Flora Disorder." Advanced Gut & Microbiome Research 2022 (October 11, 2022): 1–13. http://dx.doi.org/10.1155/2022/7883756.

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Objective. This study is aimed at analyzing the molecular mechanism of Xuanfei Baidu Granule (XFBDG) in the treatment of intestinal flora disorder based on network pharmacology. Methods. The TCMSP database was used to obtain the active components and target proteins of XFBDG, while the GeneCards database was used to obtain the related proteins of intestinal flora disorder. The Rx64 4.0.2 software was used to analyze the GO functional enrichment and KEGG pathway enrichment of drug component target protein and disease-related protein to obtain the pathway-enriched proteins and screen the core proteins for topology analysis of the pathway target by using the STRING database and Cytoscape v3.8.2 software. The Cytoscape v3.8.2 software was used to analyze the relationship between each component and enriched protein, and the AutoDock Vina software was used for molecular docking of core proteins and components. Results. XFBDG contains 133 active components that can act on 249 proteins related to intestinal flora disorder. The effects include the following: (i) regulation of functions—the response to drug, cellular response to chemical stress, response to oxidative stress, and RNA polymerase II-specific DNA-binding transcription factor binding and (ii) regulation of signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, and Th17 cell differentiation pathway. The enriched core proteins in these pathways are IFNG, IL4, PTGS2, JUN, and IL1B that set in a higher level of binding with the corresponding drug components. Conclusion. XFBDG can act on IFNG, IL4, PTGS2, JUN, and IL1B proteins through its active components such as quercetin, luteolin, and kaempferol to regulate the IL-17, TNF, and Th17 cell differentiation pathways and further regulate the response to drug, cellular response to chemical stress, response to oxidative stress, and RNA polymerase II-specific DNA-binding transcription factor binding. In addition, owing to its antioxidant and anti-inflammatory properties and related immune responses, XFBDG can achieve a balance of intestinal flora and microbial metabolism.

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Lhakhang, Tenzin W., and M. Ahmad Chaudhry. "Interactome of Radiation-Induced microRNA-Predicted Target Genes." Comparative and Functional Genomics 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/569731.

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The microRNAs (miRNAs) function as global negative regulators of gene expression and have been associated with a multitude of biological processes. The dysfunction of the microRNAome has been linked to various diseases including cancer. Our laboratory recently reported modulation in the expression of miRNA in a variety of cell types exposed to ionizing radiation (IR). To further understand miRNA role in IR-induced stress pathways, we catalogued a set of common miRNAs modulated in various irradiated cell lines and generated a list of predicted target genes. Using advanced bioinformatics tools we identified cellular pathways where miRNA predicted target genes function. The miRNA-targeted genes were found to play key roles in previously identified IR stress pathways such as cell cycle, p53 pathway, TGF-beta pathway, ubiquitin-mediated proteolysis, focal adhesion pathway, MAPK signaling, thyroid cancer pathway, adherens junction, insulin signaling pathway, oocyte meiosis, regulation of actin cytoskeleton, and renal cell carcinoma pathway. Interestingly, we were able to identify novel targeted pathways that have not been identified in cellular radiation response, such as aldosterone-regulated sodium reabsorption, long-term potentiation, and neutrotrophin signaling pathways. Our analysis indicates that the miRNA interactome in irradiated cells provides a platform for comprehensive modeling of the cellular stress response to IR exposure.

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Santiago, J., M. A. S. Santos, M. Fardilha, and J. V. Silva. "Stress response pathways in the male germ cells and gametes." Molecular Human Reproduction 26, no. 1 (December 9, 2019): 1–13. http://dx.doi.org/10.1093/molehr/gaz063.

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Abstract The unfolded protein response (UPR) is a conserved and essential cellular pathway involved in protein quality control that is activated in response to several cellular stressors such as diseases states, ageing, infection and toxins. The cytosol, endoplasmic reticulum (ER) and mitochondria are continuously exposed to new proteins and in situations of aberrant protein folding; one of three lines of defence may be activated: (i) heat-shock response, (ii) mitochondrial UPR and (iii) ER UPR. These pathways lead to different signal transduction mechanisms that activate or upregulate transcription factors that, in turn, regulate genes that increase the cell's ability to correct the conformation of poorly folded proteins or, ultimately, lead to apoptosis. Despite the recent progress in understanding such biological processes, few studies have focused on the implications of the UPR in male infertility, highlighting the need for a first approach concerning the presence of these components in the male reproductive system. In testis, there is a high rate of protein synthesis, and the UPR mechanisms are well described. However, the presence of these mechanisms in spermatozoa, apparently transcriptionally inactive cells, is contentious, and it is unclear how sperm cells deal with stress. Here, we review current concepts and mechanisms of the UPR and highlight the relevance of these stress response pathways in male fertility, especially the presence and functional activation of those components in male germinal cells and spermatozoa.

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Srikanth, Krishnamoorthy, Jong-Eun Park, Sang Yun Ji, Ki Hyun Kim, Yoo Kyung Lee, Himansu Kumar, Minji Kim, et al. "Genome-Wide Transcriptome and Metabolome Analyses Provide Novel Insights and Suggest a Sex-Specific Response to Heat Stress in Pigs." Genes 11, no. 5 (May 11, 2020): 540. http://dx.doi.org/10.3390/genes11050540.

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Heat stress (HS) negatively impacts pig production and swine health. Therefore, to understand the genetic and metabolic responses of pigs to HS, we used RNA-Seq and high resolution magic angle spinning (HR-MAS) NMR analyses to compare the transcriptomes and metabolomes of Duroc pigs (n = 6, 3 barrows and 3 gilts) exposed to heat stress (33 °C and 60% RH) with a control group (25 °C and 60% RH). HS resulted in the differential expression of 552 (236 up, 316 down) and 879 (540 up, 339 down) genes and significant enrichment of 30 and 31 plasma metabolites in female and male pigs, respectively. Apoptosis, response to heat, Toll-like receptor signaling and oxidative stress were enriched among the up-regulated genes, while negative regulation of the immune response, ATP synthesis and the ribosomal pathway were enriched among down-regulated genes. Twelve and ten metabolic pathways were found to be enriched (among them, four metabolic pathways, including arginine and proline metabolism, and three metabolic pathways, including pantothenate and CoA biosynthesis), overlapping between the transcriptome and metabolome analyses in the female and male group respectively. The limited overlap between pathways enriched with differentially expressed genes and enriched plasma metabolites between the sexes suggests a sex-specific response to HS in pigs.

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Ali, Md Sarafat, and Kwang-Hyun Baek. "Jasmonic Acid Signaling Pathway in Response to Abiotic Stresses in Plants." International Journal of Molecular Sciences 21, no. 2 (January 17, 2020): 621. http://dx.doi.org/10.3390/ijms21020621.

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Plants as immovable organisms sense the stressors in their environment and respond to them by means of dedicated stress response pathways. In response to stress, jasmonates (jasmonic acid, its precursors and derivatives), a class of polyunsaturated fatty acid-derived phytohormones, play crucial roles in several biotic and abiotic stresses. As the major immunity hormone, jasmonates participate in numerous signal transduction pathways, including those of gene networks, regulatory proteins, signaling intermediates, and proteins, enzymes, and molecules that act to protect cells from the toxic effects of abiotic stresses. As cellular hubs for integrating informational cues from the environment, jasmonates play significant roles in alleviating salt stress, drought stress, heavy metal toxicity, micronutrient toxicity, freezing stress, ozone stress, CO2 stress, and light stress. Besides these, jasmonates are involved in several developmental and physiological processes throughout the plant life. In this review, we discuss the biosynthesis and signal transduction pathways of the JAs and the roles of these molecules in the plant responses to abiotic stresses.

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Nickoloff, Jac A. "Targeting Replication Stress Response Pathways to Enhance Genotoxic Chemo- and Radiotherapy." Molecules 27, no. 15 (July 25, 2022): 4736. http://dx.doi.org/10.3390/molecules27154736.

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Proliferating cells regularly experience replication stress caused by spontaneous DNA damage that results from endogenous reactive oxygen species (ROS), DNA sequences that can assume secondary and tertiary structures, and collisions between opposing transcription and replication machineries. Cancer cells face additional replication stress, including oncogenic stress that results from the dysregulation of fork progression and origin firing, and from DNA damage induced by radiotherapy and most cancer chemotherapeutic agents. Cells respond to such stress by activating a complex network of sensor, signaling and effector pathways that protect genome integrity. These responses include slowing or stopping active replication forks, protecting stalled replication forks from collapse, preventing late origin replication firing, stimulating DNA repair pathways that promote the repair and restart of stalled or collapsed replication forks, and activating dormant origins to rescue adjacent stressed forks. Currently, most cancer patients are treated with genotoxic chemotherapeutics and/or ionizing radiation, and cancer cells can gain resistance to the resulting replication stress by activating pro-survival replication stress pathways. Thus, there has been substantial effort to develop small molecule inhibitors of key replication stress proteins to enhance tumor cell killing by these agents. Replication stress targets include ATR, the master kinase that regulates both normal replication and replication stress responses; the downstream signaling kinase Chk1; nucleases that process stressed replication forks (MUS81, EEPD1, Metnase); the homologous recombination catalyst RAD51; and other factors including ATM, DNA-PKcs, and PARP1. This review provides an overview of replication stress response pathways and discusses recent pre-clinical studies and clinical trials aimed at improving cancer therapy by targeting replication stress response factors.

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Abdelwahed, Eman K., Nahla A. Hussein, Ahmed Moustafa, Nayera A. Moneib, and Ramy K. Aziz. "Gene Networks and Pathways Involved in Escherichia coli Response to Multiple Stressors." Microorganisms 10, no. 9 (September 6, 2022): 1793. http://dx.doi.org/10.3390/microorganisms10091793.

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Stress response helps microorganisms survive extreme environmental conditions and host immunity, making them more virulent or drug resistant. Although both reductionist approaches investigating specific genes and systems approaches analyzing individual stress conditions are being used, less is known about gene networks involved in multiple stress responses. Here, using a systems biology approach, we mined hundreds of transcriptomic data sets for key genes and pathways involved in the tolerance of the model microorganism Escherichia coli to multiple stressors. Specifically, we investigated the E. coli K-12 MG1655 transcriptome under five stresses: heat, cold, oxidative stress, nitrosative stress, and antibiotic treatment. Overlaps of transcriptional changes between studies of each stress factor and between different stressors were determined: energy-requiring metabolic pathways, transport, and motility are typically downregulated to conserve energy, while genes related to survival, bona fide stress response, biofilm formation, and DNA repair are mainly upregulated. The transcription of 15 genes with uncharacterized functions is higher in response to multiple stressors, which suggests they may play pivotal roles in stress response. In conclusion, using rank normalization of transcriptomic data, we identified a set of E. coli stress response genes and pathways, which could be potential targets to overcome antibiotic tolerance or multidrug resistance.

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Luo, Min, and Mei-ling A. Joiner. "Stress Response Signaling Pathways May Lead to Mitochondrial Biogenesis." Diabetes 63, no. 6 (May 22, 2014): 1831–32. http://dx.doi.org/10.2337/db14-0373.

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Song, G., G. G. Chen, T. Hu, and P. B. S. Lai. "Bid Stands at the Crossroad of Stress-Response Pathways." Current Cancer Drug Targets 10, no. 6 (September 1, 2010): 584–92. http://dx.doi.org/10.2174/156800910791859515.

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Kourtis, Nikos, and Nektarios Tavernarakis. "Cellular stress response pathways and ageing: intricate molecular relationships." EMBO Journal 30, no. 13 (May 17, 2011): 2520–31. http://dx.doi.org/10.1038/emboj.2011.162.

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Farley, Madeline M., and Trent A. Watkins. "Intrinsic Neuronal Stress Response Pathways in Injury and Disease." Annual Review of Pathology: Mechanisms of Disease 13, no. 1 (January 24, 2018): 93–116. http://dx.doi.org/10.1146/annurev-pathol-012414-040354.

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Tesh, Vernon L. "Activation of cell stress response pathways by Shiga toxins." Cellular Microbiology 14, no. 1 (September 22, 2011): 1–9. http://dx.doi.org/10.1111/j.1462-5822.2011.01684.x.

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Myers, Shirley M., and Lois M. Mulligan. "The RET Receptor Is Linked to Stress Response Pathways." Cancer Research 64, no. 13 (July 1, 2004): 4453–63. http://dx.doi.org/10.1158/0008-5472.can-03-3605.

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Martin, Humberto, Michael Shales, Pablo Fernandez‐Piñar, Ping Wei, Maria Molina, Dorothea Fiedler, Kevan M. Shokat, Pedro Beltrao, Wendell Lim, and Nevan J. Krogan. "Differential genetic interactions of yeast stress response MAPK pathways." Molecular Systems Biology 11, no. 4 (April 2015): 800. http://dx.doi.org/10.15252/msb.20145606.

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Gotoh, Tomomi, Motoyoshi Endo, and Yuichi Oike. "Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases." International Journal of Inflammation 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/259462.

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The endoplasmic reticulum (ER) is the site of synthesis and maturation of proteins designed for secretion or for localization on the cell membrane. Various types of stress from both inside and outside cells disturb ER function, thus causing unfolded or misfolded proteins to accumulate in the ER. To improve and maintain the ER functions against such stresses, the ER stress response pathway is activated. However, when the stress is prolonged or severe, apoptosis pathways are activated to remove damaged cells. It was recently reported that the ER stress pathway is also involved in the inflammatory response, whereby inflammation induces ER stress, and ER stress induces an inflammatory response. Therefore, the ER stress response pathway is involved in various diseases, including cardiovascular diseases such as atherosclerosis and ischemic diseases, in various ways. The ER stress pathway may represent a novel target for the treatment of these diseases.

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Journal articles on the topic 'Stress response pathways'

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