Flavonoid-induced apoptosis pathway

The "Flavonoid-induced apoptosis pathway" encompasses the molecular and cellular signaling routes by which flavonoids stimulate programmed cell death in cancer and other cells. This involves both extrinsic (death receptor-mediated, such as activation of Fas and TNF receptors) and intrinsic (mitochondrial-mediated, such as Bcl-2 family regulation and cytochrome c release) apoptotic pathways. Flavonoids activate the caspase cascade, promote mitochondrial membrane permeabilization, trigger cytochrome c and apoptosome formation, modulate key regulatory proteins (p53, Bcl-2, Bcl-xL, Bax), and may generate reactive oxygen species. These coordinated events lead to chromatin condensation, DNA fragmentation, and cell death, with important implications for anti-cancer therapy[2][3][5][6]. This pathway is a mechanism-of-action for a class of compounds but does not itself constitute a druggable molecular target.

Other names

Flavonoid-mediated apoptosis pathwayFlavonoid-triggered apoptotic signalingFlavonoid-induced cell death pathway

Induction of intrinsic (mitochondrial) apoptosis pathway (modulation of Bcl-2 family proteins, Bax/Bcl-xL ratio, cytochrome c release) Induction of extrinsic (death receptor-mediated) apoptosis pathway (activation of Fas/TNF receptor family, caspase-8 activation) Activation of caspases (3, 7, 8, and 9) Inhibition of PI3K/Akt and MAPK signaling ROS generation and DNA damage[1][2][3][5][6]