Endosyttoosi

Endosyttoosi, or endocytosis, is a cellular process by which cells internalize extracellular material by enveloping it with the plasma membrane to form vesicles. It enables nutrient uptake, membrane turnover, and regulation of signaling pathways, and is fundamental to cellular homeostasis.

There are several main forms of endocytosis. Phagocytosis involves the ingestion of large particles such as microbes or dead cells. Pinocytosis captures extracellular fluid and solutes in small vesicles, typically in a non-specific manner. Receptor-mediated endocytosis is highly specific and relies on cell-surface receptors binding ligands, followed by internalization. This pathway often uses clathrin-coated pits and adaptor proteins, with dynamin helping to pinch off vesicles. Other routes include caveolin-mediated endocytosis and various clathrin- and caveolin-independent mechanisms.

The process generally proceeds through binding, vesicle formation, and vesicle scission, followed by uncoating and trafficking to early endosomes. Sorting decides the fate of internalized material: some is recycled back to the plasma membrane, others are sent to late endosomes and lysosomes for degradation. Rab GTPases regulate vesicle trafficking, while SNARE proteins mediate vesicle fusion with target membranes.

Biological roles of endocytosis are diverse. It enables uptake of nutrients such as iron and cholesterol, regulates surface receptor levels and signaling sensitivity, and supports immune defense through phagocytosis. Many pathogens exploit endocytosis to gain cell entry, which can contribute to infection. Abnormal endocytic activity is associated with diseases, including dyslipidemias (e.g., faulty LDL receptor–mediated uptake) and certain neurodegenerative conditions where endocytic trafficking is disrupted.

Endosyttoosi is a dynamic and essential process that integrates membrane traffic, signaling, and metabolism across cell types.