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Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Graier, WF; Malli, R; Kostner, GM.
Mitochondrial protein phosphorylation: instigator or target of lipotoxicity?
Trends Endocrinol Metab. 2009; 20(4): 186-193.
Doi: 10.1016/j.tem.2009.01.004
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- Führende Autor*innen der Med Uni Graz
- Graier Wolfgang
- Co-Autor*innen der Med Uni Graz
- Kostner Gerhard
- Malli Roland
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- Abstract:
- Lipotoxicity occurs as a consequence of chronic exposure of non-adipose tissue and cells to elevated concentrations of fatty acids, triglycerides and/or cholesterol. The contribution of mitochondria to lipotoxic cell dysfunction, damage and death is associated with elevated production of reactive oxygen species and initiation of apoptosis. Although there is a broad consensus on the involvement of these phenomena with lipotoxicity, the molecular mechanisms that initiate, mediate and trigger mitochondrial dysfunction in response to substrate overload remain unclear. Here, we focus on protein phosphorylation as an important phenomenon in lipotoxicity that harms mitochondria-related signal transduction and integration in cellular metabolism. Moreover, the degradation of mitochondria by mitophagy is discussed as an important landmark that leads to cellular apoptosis in lipotoxicity.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Apoptosis -
- Dietary Fats - adverse effects
- Humans -
- Mitochondria - metabolism
- Mitochondrial Proteins - metabolism
- Models, Biological -
- Phosphorylation -
- Signal Transduction - physiology