Abstract:
Abstract.Apoptosis and necroptosis are key forms of programmed cell death that play a crucial role in maintaining homeostasis and controlling pathological processes in the human body. Dysregulation of these mechanisms can lead to the development of a wide range of diseases, including oncological, neurodegenerative, autoimmune and inflammatory conditions. Apoptosis is characterized by the activation of caspases and the formation of morphological changes, which ensures the controlled removal of damaged cells, while necroptosis is triggered through the RIPK1/RIPK3/MLKL signaling pathways and is accompanied by the release of pro-inflammatory mediators. The relevance of the topic is due to the need for a deeper understanding of the molecular basis of cell death and their significance for the pathogenesis of diseases and therapeutic strategies. The aim of the work is to systematize modern scientific data on the mechanisms of apoptosis and necroptosis and their contribution to the development of human pathologies. Materials and methods. To achieve this goal, a targeted search and analysis of scientific publications over the past 10 years was conducted in the PubMed, Scopus and Google Scholar databases. Sources were selected using the following keywords: "apoptosis", "necroptosis", "cell death", "pathogenesis", "molecular pathways", "inflammation", "therapeutic targets". The analysis included experimental and clinical studies that highlight the role of cell death signaling pathways in the development of diseases. Results. The literature review confirmed that apoptosis is a central mechanism for controlling cell proliferation and preventing tumor transformation. Dysfunction of the caspase cascade is associated with resistance to therapy in oncology. Necroptosis, on the contrary, plays an important role in the development of inflammatory processes, since the release of cellular contents upon its activation stimulates the immune response. It was noted that the activation of RIPK3 and MLKL is closely related to the severity of neurodegenerative diseases. In addition, there is evidence of cross-regulation between apoptosis and necroptosis, which provides flexibility of cellular responses in response to stressful stimuli. Studies also show that pharmacological modulation of these pathways opens up prospects for new therapeutic approaches. Conclusions. Apoptosis and necroptosis are interconnected mechanisms of cell death, which are of fundamental importance for the development of pathological conditions. Understanding their molecular basis allows us to explain the pathogenesis of many diseases and identifies new directions for therapy. Further research in this area is promising for the creation of innovative drugs aimed at the selective regulation of cell death.
