Cytostase

Cytostase, also known as cytostasis, refers to the arrest of cell growth and division while maintaining cellular viability. In this state, cells stop progressing through the cell cycle rather than dying, and metabolic activity may continue at a reduced or altered level. Cytostasis can occur as a normal regulatory process or be induced by external factors such as drugs, nutrients, or environmental stress. It is distinct from cytotoxicity or cytolysis, which involve cell killing.

The mechanisms of cytostase involve cell cycle control and signaling pathways that halt progression at checkpoints. Common targets include cyclin-dependent kinases, the retinoblastoma (Rb) pathway, and the p53–p21 axis. Arrest can occur at various stages, typically G1, S, or G2, depending on the stimulus. Cytostatic effects may be reversible, allowing cells to re-enter the cycle if the arresting condition is removed, or irreversible, leading to senescence or programmed cell death if damage or stress persists.

Applications and implications of cytostasis are widespread. In physiology, cytostatic states help regulate tissue growth and maintain homeostasis. In medicine, cytostatic (cytostatic) drugs are used to slow tumor growth by stopping cancer cell proliferation, rather than immediately killing cells. In research, cytostasis is studied to evaluate drug efficacy and mechanisms of cell-cycle control, with assessment methods including cell-cycle analysis by flow cytometry, DNA synthesis measurements, and viability assays.

Terminology notes: cytostasis is often contrasted with cytotoxicity (cell killing) and cytolysis (cell rupture).