sejthalál

Sejthalál, or cell death, is the process by which a cell ceases to live and is removed from a tissue. It is a fundamental biological phenomenon that can be physiological, supporting development and tissue turnover, or pathological, contributing to disease. Sejthalál is generally categorized as programmed (regulated) death or as uncontrolled death resulting from acute injury.

The most studyied form is apoptosis, a programmed process driven by intracellular signaling pathways that activate caspases. It can occur via intrinsic pathways, often involving mitochondrial outer membrane permeabilization and cytochrome c release, or via extrinsic pathways triggered by death receptors on the cell surface. Apoptosis typically features cell shrinkage, chromatin condensation, DNA fragmentation, and orderly phagocytosis without provoking inflammation. Other programmed forms of sejthalál include necroptosis and pyroptosis, which are inflammatory and regulated by distinct signaling cascades, and ferroptosis, an iron-dependent form characterized by lipid peroxidation. Autophagic cell death is discussed in the literature as a form where autophagy contributes to cell demise, sometimes in conjunction with apoptosis.

In contrast, necrosis is an uncontrolled form of cell death arising from severe injury, leading to cell swelling, membrane rupture, and inflammation. Recognition and measurement of sejthalál employ various markers and assays, such as morphological assessment, TUNEL staining for DNA fragmentation, Annexin V binding, and caspase activity assays.

Understanding sejthalál has wide implications for medicine, including cancer therapy that aims to induce cancer cell death, and diseases where excessive or insufficient sejthalál contributes to tissue damage, neurodegeneration, or ischemia-reperfusion injury. See also apoptosis, necrosis, autophagy, necroptosis, ferroptosis.