Apoptosisisaformofgeneticallyprogrammedcelldeath,whichplaysakeyroleinregulationofcellularityinavarietyoftissueandcelltypesincludingthecardiovasculartissues.Underbothphysiologicalandpathophysiologicalconditions,variousbiophysiologicalandbiochemicalfactors,includingmechanicalforces,reactiveoxygenandnitrogenspecies,cytokines,growthfactors,oxidizedlipoproteins,etc.,mayinfluenceapoptosisofvascularcells.TheFas/Fasligand/caspasedeath-signalingpathway,Bcl-2proteinfamily/mitochondria,thetumorsuppressivegenep53,andtheproto-oncogenec-mycmaybeactivatedinatheroscleroticlesions,andmediatesvascularapoptosisduringthedevelopmentofatherosclerosis.Abnormalexpressionanddysfunctionoftheseapoptosis-regulatinggenesmayattenuateoracceleratevascularcellapoptosisandaffecttheintegrityandstabilityofatheroscleroticplaques.Clarificationofthemolecularmechanismthatregulatesapoptosismayhelpdesignanewstrategyfortreatmentofatherosclerosisanditsmajorcomplication,theacutevascularsyndromes.
