Senescence in the population of cells is often described as a program of restricted proliferative capacity, which is manifested by broad morphological and biochemical changes including a metabolic shift towards an autophagic-like response and a genotoxic-stress related induction of polyploidy. Concomitantly, the cell cycle progression of a senescent cell is believed to be irreversibly arrested. Recent reports suggest that this phenomenon may have an influence on the therapeutic outcome of anticancer treatment. The aim of this study was to verify the possible involvement of this program in the response to the treatment of the A549 cell population with low doses of etoposide, as well as to describe accompanying cytoskeletal alterations.

Homeostasis is a fundamental property of biological systems consisting of the ability to maintain a dynamic balance of the environment of biochemical processes. The action of endogenous and exogenous factors can lead to internal balance disorder, which results in the activation of the immune system and the development of inflammatory response. Inflammation determines the disturbances in the structure of the vessel wall, connected with the change in their diameter. These disorders consist of accumulation in the space between the endothelium and the muscle cells of low-density lipoproteins (LDL), resulting in the formation of fatty streaks narrowing the lumen and restricting the blood flow in the area behind the structure. The effect of inflammation may also be pathological dilatation of the vessel wall associated with the development of aneurysms. Described disease entities strongly correlate with the increased migration of immune cells. Recent scientific research indicates the secretion of specific vesicular structures during migration activated by the inflammation. The review focuses on the link between endothelial dysfunction and the inflammatory response and the impact of these processes on the development of disease entities potentially related to the secretion of extracellular vesicles (EVs).

Glial cells have emerged as active and dynamic regulators of central nervous system (CNS) function, far beyond their historically perceived supportive role. This review synthesizes the most recent advances in glial biology, highlighting novel molecular mechanisms, cutting-edge imaging methodologies, and translational strategies that redefine their role in health and disease. We emphasize new findings on astrocytic signaling in neurodegeneration, NG2-glia dynamics, and microglial modulation, providing forward-looking perspectives for glia-targeted therapeutic interventions. Recent breakthroughs in high-resolution in vivo imaging, single-cell transcriptomics, and gene-editing platforms are discussed in the context of their ability to unravel glial heterogeneity and functional plasticity. By integrating molecular insights with translational research, this review aims to bridge the gap between basic neuroscience and clinical applications, offering a framework for next-generation CNS therapies.