Host-cell autophagy pathway (Autophagy)

Autophagy is a fundamental, evolutionarily conserved intracellular process that mediates the degradation and recycling of cytoplasmic components, including damaged organelles and misfolded proteins, through the lysosomal pathway [1.1.2, 1.2.1]. It serves as a critical homeostatic mechanism, allowing cells to survive under stress conditions such as nutrient deprivation by generating metabolic precursors [1.1.4, 1.2.5]. In the context of human health, host-cell autophagy pathways are involved in a wide range of diseases, including cancer, neurodegeneration, and infectious diseases [1.1.2, 1.2.2]. For example, autophagy can act as a defense mechanism against intracellular pathogens (xenophagy) or as a quality control system to prevent the accumulation of toxic protein aggregates in neurons [1.1.1, 1.4.2]. However, its role is often dualistic; in cancer, it can suppress early tumor formation but support the survival of established tumors under metabolic stress [1.1.3, 1.3.5]. Therapeutic modulation of autophagy involves either activating the pathway using mTOR inhibitors or AMPK activators or inhibiting it using lysosomotropic agents like chloroquine [1.3.2, 1.4.4]. Despite its potential, targeting autophagy remains challenging due to the lack of specific biomarkers and the risk of off-target effects in healthy tissues [1.4.4].

Other names

MacroautophagyMicroautophagyChaperone-mediated autophagyXenophagyAutophagy-lysosome pathway

Modulation of autophagic flux through mTOR inhibition, AMPK activation, or lysosomal function disruption [1.3.2, 1.4.4].