▁production ▁of ▁prote ins ▁within ▁cells , ▁become ▁activ ated ; ▁specifically ▁AP - 1 ▁and ▁N F - κ B , ▁leading ▁to ▁increased ▁expression ▁of ▁cy tok ines ▁such ▁as ▁IL - 1 , ▁T NF α ▁and ▁IF N γ , ▁which ▁prom otes ▁infl amm ation . ▁This ▁state ▁of ▁end oth el ial ▁cells ▁prom otes ▁accum ulation ▁of ▁lip ids ▁and ▁li pop rote ins ▁in ▁the ▁int ima , ▁leading ▁to ▁a ther os cl eros is , ▁and ▁the ▁subsequent ▁rec ruit ment ▁of ▁white ▁blood ▁cells ▁and ▁plate lets , ▁as ▁well ▁as ▁pro l ifer ation ▁of ▁smooth ▁mus cle ▁cells , ▁leading ▁to ▁the ▁formation ▁of ▁a ▁fat ty ▁stre ak . ▁The ▁les ions ▁formed ▁in ▁the ▁int ima , ▁and ▁persistent ▁infl amm ation ▁lead ▁to ▁des qu am ation ▁of ▁end oth el ium , ▁which ▁dis rupt s ▁the ▁end oth el ial ▁bar rier , ▁leading ▁to ▁injury ▁and ▁consequ ent ▁d ys function . ▁In ▁contrast , ▁infl am mat ory ▁stim uli ▁also ▁activ ate ▁N F - κ B - indu ced ▁expression ▁of ▁the ▁de ub iqu it in ase ▁A 2 0 ▁( T N FA IP 3 ), ▁which ▁has ▁been ▁shown ▁to ▁intr ins ically ▁repair ▁the ▁end oth el ial ▁bar rier ▁. ▁▁▁ ▁One ▁of ▁the ▁main ▁mechan isms ▁of ▁end oth el ial ▁d ys function ▁is ▁the ▁dimin ishing ▁of ▁nit ric ▁ox ide , ▁often