Endothelial cell autophagy pathway

Endothelial cell autophagy is a conserved intracellular degradation pathway in which cytoplasmic components are delivered via autophagosomes to lysosomes for breakdown and recycling. In endothelial cells, this pathway regulates cellular homeostasis, energy adaptation, redox balance, senescence, vascular integrity, and pathological responses in diseases such as atherosclerosis, cancer, and inflammation[1][3][5][7]. Autophagy is regulated by master switches such as mTOR, AMPK, ULK1, and multiple stress signaling pathways[2][5]. Modulation of endothelial autophagy influences vascular disease progression and is a potential (though non-specific and broad) therapeutic avenue, but the pathway itself is not a singular druggable target — rather, drugs like rapamycin or chloroquine broadly modulate this cellular process[2][6][7]. Accordingly, "endothelial cell autophagy pathway" is not a canonical therapeutic target but denotes a cell process involving many molecules.

Other names

Endothelial autophagyEC autophagyAutophagy in endothelial cells

mTOR inhibition (induces autophagy, e.g., by rapamycin); Lysosomal inhibition (blocks autophagy flux, e.g., by chloroquine); AMPK activation; ULK1 pathway modulation