The evolution of the concept of stress and the framework of the stress system

Lu, Siyu; Wei, Fang; Li, Guolin

doi:10.15698/cst2021.06.250

Cited by 93 publications

(62 citation statements)

References 91 publications

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“…This pro-survival response allows the body to face and deal with the challenge and re-establish homeostatic equilibrium, promoting health. However, if the individual perceives a noxious stimulus as too intense, or its duration as too long, they may fail to cope with it, maladaptation occurs, neuroimmunoendocrine parameters remain altered, accelerating the rate of aging and the appearance of age-related diseases [ 4 , 85 , 86 ]. In accordance with this, there are several examples in which chronic stress situations were associated with a defective immune functional capacity [ 87 , 88 , 89 ] and with accelerated aging [ 4 , 90 ].…”

Section: Lifestyle Situations Modulating the Rate Of Aging: Friends Or Foes?mentioning

confidence: 99%

The Role of Immune Cells in Oxi-Inflamm-Aging

Toda

Ceprián

Cerro

et al. 2021

Cells

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Aging is the result of the deterioration of the homeostatic systems (nervous, endocrine, and immune systems), which preserve the organism’s health. We propose that the age-related impairment of these systems is due to the establishment of a chronic oxidative stress situation that leads to low-grade chronic inflammation throughout the immune system’s activity. It is known that the immune system weakens with age, which increases morbidity and mortality. In this context, we describe how the function of immune cells can be used as an indicator of the rate of aging of an individual. In addition to this passive role as a marker, we describe how the immune system can work as a driver of aging by amplifying the oxidative-inflammatory stress associated with aging (oxi-inflamm-aging) and inducing senescence in far tissue cells. Further supporting our theory, we discuss how certain lifestyle conditions (such as social environment, nutrition, or exercise) can have an impact on longevity by affecting the oxidative and inflammatory state of immune cells, regulating immunosenescence and its contribution to oxi-inflamm-aging.

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Section: Lifestyle Situations Modulating the Rate Of Aging: Friends Or Foes?mentioning

confidence: 99%

The Role of Immune Cells in Oxi-Inflamm-Aging

Toda

Ceprián

Cerro

et al. 2021

Cells

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“…Cell stress can be anything that disrupts the homeostatic balance of normal cells, such as reactive oxygen species, bacterial toxins, changes in osmolarity, DNA damage, etc. Equipped with stress response pathways, including p38 signaling, cells adjust to these challenges to maintain cell function [14]. Once activated, the p38 signal cascade regulates the cell cycle by influencing both the timing of cell cycle entry and cell cycle checkpoint arrests that are necessary for cells to adjust to their environment.…”

Section: P38 Signaling and Cell Cycle Regulationmentioning

confidence: 99%

Stress Relief Techniques: p38 MAPK Determines the Balance of Cell Cycle and Apoptosis Pathways

Whitaker¹,

Cook²

2021

Biomolecules

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Protein signaling networks are formed from diverse and inter-connected cell signaling pathways converging into webs of function and regulation. These signaling pathways both receive and conduct molecular messages, often by a series of post-translation modifications such as phosphorylation or through protein–protein interactions via intrinsic motifs. The mitogen activated protein kinases (MAPKs) are components of kinase cascades that transmit signals through phosphorylation. There are several MAPK subfamilies, and one subfamily is the stress-activated protein kinases, which in mammals is the p38 family. The p38 enzymes mediate a variety of cellular outcomes including DNA repair, cell survival/cell fate decisions, and cell cycle arrest. The cell cycle is itself a signaling system that precisely controls DNA replication, chromosome segregation, and cellular division. Another indispensable cell function influenced by the p38 stress response is programmed cell death (apoptosis). As the regulators of cell survival, the BCL2 family of proteins and their dynamics are exquisitely sensitive to cell stress. The BCL2 family forms a protein–protein interaction network divided into anti-apoptotic and pro-apoptotic members, and the balance of binding between these two sides determines cell survival. Here, we discuss the intersections among the p38 MAPK, cell cycle, and apoptosis signaling pathways.

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“…It is used as a marker of how much psychological and social stressors impact biological functioning [7][8][9]. Allostatic load values reflect chronic, steady state levels of stress as well as failure to terminate responses to acute stressors [10,11].…”

Section: Introductionmentioning

confidence: 99%

A Systems Approach to Interrogate Gene Expression Patterns in African American Men Presenting with Clinically Localized Prostate Cancer

Hardiman

Savage

Hazard

et al. 2021

Cancers

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An emerging theory about racial differences in cancer risk and outcomes is that psychological and social stressors influence cellular stress responses; however, limited empirical data are available on racial differences in cellular stress responses among men who are at risk for adverse prostate cancer outcomes. In this study, we undertook a systems approach to examine molecular profiles and cellular stress responses in an important segment of African American (AA) and European American (EA) men: men undergoing prostate biopsy. We assessed the prostate transcriptome with a single biopsy core via high throughput RNA sequencing (RNA-Seq). Transcriptomic analyses uncovered impacted biological pathways including PI3K-Akt signaling pathway, Neuroactive ligand-receptor interaction pathway, and ECM-receptor interaction. Additionally, 187 genes mapping to the Gene Ontology (GO) terms RNA binding, structural constituent of ribosome, SRP-dependent co-translational protein targeting to membrane and the biological pathways, translation, L13a-mediated translational silencing of Ceruloplasmin expression were differentially expressed (DE) between EA and AA. This signature allowed separation of AA and EA patients, and AA patients with the most severe clinical characteristics. AA patients with elevated expression levels of this genomic signature presented with higher Gleason scores, a greater number of positive core biopsies, elevated dehydroepiandrosterone sulfate levels and serum vitamin D deficiency. Protein-protein interaction (PPI) network analysis revealed a high degree of connectivity between these 187 proteins.

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The evolution of the concept of stress and the framework of the stress system

Cited by 93 publications

References 91 publications

The Role of Immune Cells in Oxi-Inflamm-Aging

The Role of Immune Cells in Oxi-Inflamm-Aging

Stress Relief Techniques: p38 MAPK Determines the Balance of Cell Cycle and Apoptosis Pathways

A Systems Approach to Interrogate Gene Expression Patterns in African American Men Presenting with Clinically Localized Prostate Cancer

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