The Effect of Chronic Stress on Apoptosis Regulation and Oncogenesis Evolution: A Theoretical Approach.
Creators: name: KIMOGLOU, DIMITRIOS
Publisher: name: figshare
Year: 2025
Subjects: classificationCode: 429999
subject: Other health sciences not elsewhere classified

description: The Effect of Chronic Stress on Apoptosis Regulation and Oncogenesis Evolution: A Theoretical Approach.Author/researcher: Dr. Dimitrios C. Kimoglou, PhD, Metropolitan Institute. Aridea Pellas Greece,Apoptosis is a regulated, physiological process of cell death that plays an important role.<br>maintains cellular homeostasis. This mechanism causes irreversible changes in cells. DNA damage or finished biological cycles are eliminated. This prohibits.the buildup of altered or defective cells that may turn into Neoplastic formations.However, in situations of extended stress, this natural regulatory system can become highly dysfunctional. The hypothalamic, pituitary, and adrenaline axis (HPA), It is responsible for the body's response to stress, is constantly active,<br>Cortisol and catecholamines (such as adrenaline) are overproduced.<br>noradrenaline). These hormones work through receptors in cells, affecting essentialSignalling circuits that control cell survival and death.Cortisol, while momentarily protective in acute situations, when produced at high levels<br>levels over an extended period of time, has an unfavorable influence on the mitochondrial membraneInhibiting the release of cytochrome C, a crucial component that activates caspase-9, causes apoptosis via the endogenous route. Additionally, catecholamines activate. Signaling pathways like NF-κB promote the creation of pro-<br>inflammatory factors and decreases cells' apoptotic sensitivity. This modification causes a buildup of cells with genetic abnormalities that would normally have Apoptosis has removed the cells.The current work aims to expand our understanding of molecular pathways.<br>Chronic stress disrupts the apoptotic process and contributes to<br>tumorigenesis. In particular, we seek to illustrate the epigenetic influence of stress on genes that control apoptosis, as well as the significance of the HPA axis as a therapeutic target for restoring cellular equilibrium. At the same time, the importance of a holistic approach to oncological care, including the management of psychological burden as part of the overall cancer treatment strategy, is emphasized. Transition from Introduction to Mechanisms Analysis.To investigate the relationship between chronic stress and apoptotic malfunction, a multilayered strategy is required that focuses on the molecular processes affected by persistent stress hormone overactivation. Following the introduction, the analysis focuses on the physiological axes and molecular pathways involved in this process, explaining how hypothalamic-pituitary-adrenal axis (HPA) activation, oxidative stress, immunosuppression, and epigenetic modifications cause apoptosis to be deregulated and contribute to the development of pathological conditions such as tumorgenesis.Simultaneously, additional aspects that have a critical influence in the body's inflammatory response and physical fragility are considered:<br>- Chronic Inflammation: Prolonged stimulation of the immune system by inflammatory cytokines causes cellular damage and promotes carcinogenesis via increased oxidative stress and angiogenesis.- Epigenetic Modifications: Changes in DNA methylation, histone acetylation, and microRNA malfunction cause the silence of key genes that govern apoptosis and tumor suppression.<br>- Social Isolation and Immunosuppression: Eliminating social interactions and social support increases the action of glucocorticoids and catecholamines, reducing natural immunological defenses. This reduces immune surveillance and leads to uncontrolled proliferation of cells with genetic defects.- Somatisation and Organ Response: Chronic stress is frequently somatised by increased autonomic nervous system activity, which causes malfunction in important organs, increases inflammation, and increases the risk of neoplastic diseases.As a result of examining these pathways, it appears that the combined action of inflammation, immunological suppression, epigenetic changes, and the organic response to psychological variables may serve as the foundation for the idea relating chronic stress to cancer. The following presentation describes these pathways in depth, provides clinical data, and conducts biochemical investigations, all of which contribute to a better understanding of the link between mental health and cellular malfunction.