Autophagy in classical monocytes

Autophagy in classical monocytes refers to the intracellular degradation and recycling mechanism occurring within the CD14++ CD16- subset of human monocytes (or Ly6Chigh monocytes in mice). This biological process is essential for maintaining cellular homeostasis, regulating energy metabolism, and controlling the secretion of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β) (Zhang et al., 2015, Nature). In classical monocytes, autophagy also plays a critical role in their survival and subsequent differentiation into macrophages or dendritic cells during an inflammatory response. Dysregulation or impairment of this pathway is heavily implicated in the pathogenesis of chronic inflammatory conditions, most notably atherosclerosis, where defective autophagy leads to mitochondrial oxidative stress and inflammasome overactivation (Evans et al., 2018, Frontiers in Immunology). While pharmacological agents like mTOR inhibitors (e.g., Rapamycin) or lysosomal inhibitors (e.g., Hydroxychloroquine) can modulate this process, 'Autophagy in classical monocytes' is classified as a biological pathway or cellular state rather than a single druggable molecular target such as a specific protein or receptor.

Other names

Monocyte macroautophagyMacroautophagy in CD14++ monocytesAutophagic flux in classical monocytes

Modulation of the autophagy-lysosome pathway through mTORC1 inhibition (to induce autophagy) or lysosomal acidification inhibition (to block autophagic flux).