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Rubelj 2018 MiP2018
Diseases Aging;senescence  +
Has abstract [[Image:MITOEAGLE-logo.jpg|left|100px|link
[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] The fundamental property of somatic cells in higher mammals is their limited division capacity ending in cellular senescence. Two main mechanisms contribute to cellular senescence, telomere shortening and damaging effects of free radicals, mostly generated by mitochondria. It is well established that these two mechanisms are in mutual interactions but many aspects of these interactions still remain to be elucidated. This was clearly demonstrated in the experiments in which cell growth and senescence, as well as telomere shortening are directly dependent on oxygen partial pressure [1]. However, expression of telomerase (TERT), an enzyme that extends telomeres, recovers cells from senescence and restores mitochondrial function. This includes TERT translocation from the nucleus and localisation to mitochondria. It appears that TERT protects mitochondria from hyperoxia-induced damage in a way that both mitochondrial DNA damage and superoxide production decrease and the mitochondrial membrane potential elevates. Also these cells have enhanced resistance to apoptosis [2]. This lecture will present new findings in research on cell senescence, aging and rejuvenation and the role of mitochondria in these processes.
e role of mitochondria in these processes.  +
Has editor [[Plangger M]]  + , [[Kandolf G]]  +
Has title [[File:RubeljI.JPG|left|90px|Ivica Rubelj]] Role of mitochondria in mammalian senescence and aging.  +
MiP area mtDNA;mt-genetics  + , mt-Medicine  +
Was submitted in year 2018  +
Was submitted to event MiP2018/MitoEAGLE Jurmala LV +
Was written by Nanic L + , Rubelj I +
Categories Abstracts
Modification date
"Modification date" is a predefined property that corresponds to the date of the last modification of a subject and is provided by Semantic MediaWiki.
07:40:57, 20 August 2018  +
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