Author/Editor | Jezernik, Kristijan | |
Title | Apoptoza | |
Translated title | Apoptosis | |
Type | članek | |
Source | Med Razgl | |
Vol. and No. | Letnik 38, št. 1 | |
Publication year | 1999 | |
Volume | str. 69-81 | |
Language | slo | |
Abstract | Apoptosis is programmed cell death occurring as a result of a genetic program activated by developmental and environmental stimuli. Apoptosis is a normal physiological event. Disregulation of the genetic programme for apop- tosis can trigger pathologic events, embryonic lethality, changes of postnatal development and increased risk of cancer. Therapeutic agents affecting the regulation of apoptosis open new possibilities of treatment of a number of apoptosis-induced diseases, including cancer. When cellular degeneration is a resutt of a disease process, recovery may be obtained by either inducing or inhibiting apoptosis. Recently, new apoptosis-regulating genes have been identified, which may provide targets for many drugs developed to treat apoptosis-induced diseases. | |
Summary | Apoptoza je programirana celična smrt, kjer določeni dražljaji v razvoju ali dražljaji iz okolja vključijo genski program, ki preko specifičnih dogodkov vodi v razgradnjo in celično smrt. Apoptoza je normalen razvojni, torej fi- ziološki proces. Napačno uravnavanje genskega programa apoptoze pa lahko pripelje do patoloških sprememb, tudi do visoke dovzetnosti za rakasta obolenja. Terapevtiki, ki spreminjajo uravnavanje apoptoze, ponujajo možnost zdravIjenja apoptotsko pogojenih bolezni. Povsod, kjer je celična degeneracija rezultat nekega obolenja, je lahko sproženje ali zaviranje apoptoze pot k ozdravijenju. Zato je treba poznati mehanizme uravnavanja apoptoze. Nedavno so bili odkriti mnogi geni, katerih produkti uravnavajo apoptozo. Mnogi geni, ki nadzorujejo apoptozo, so konzervativni in vsesplošni v živem svetu. Ti geni so lahko tarčno mesto delovanja mnogih učinkovin in s tem vplivanja na obolevni proces. | |
Descriptors | APOPTOSIS GENES, BCL-2 GENES, P53 GENES, MYC GENES, FOS GENES, JUN |