Ageing and inflammation, key contributors to vascular dysfunction, are also associated with the impairment of mitochondrial function. Multiple known mitochondria related mechanisms could affect vascular function. However, the functional conseąuences of metabolic pathways alterations in the regulation of NO-dependent function in basal conditions, ageing, and vascular inflammation remain unclear. The primary objective of this PhD thesis was therefore to assess the role of yascular mitochondrial bioenergetic metabolism in maintaining endothelial function, with a focus on the contributions of ageing and vascular inflammation. In summary, the results presented in this PhD thesis demonstrated the pivotal function of vascular mitochondrial metabolism in preserving endothelial function, in contrast to glycolysis in the vascular wali. The deterioration of vascular phenotype and function in ageing was associated with decreased NAD pool and impaired mitochondrial and glycolytic capacity. The age-dependent impaired vascular metabolic flexibility in response to acute proinflammatory stimuli was closely associated with metabolic reprogramming towards the increased activity of pentose phosphate pathway (PPP) and decreased pyruvate oxidation, which contributed to the vascular dysfunction in the setting ofinflammation. Finally, inhibition of PPP in the aorta of old mice improved vascular functi ; on, but in the young mice this effect was not observed, likely to a preseryed adaptiye metabolic response to inflammation in the young aorta.
Rada Dyscypliny Nauki medyczne
Chłopicki, Stefan ; Kaczara, Patrycja
Feb 27, 2026
Feb 27, 2026
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http://dl.bm.cm-uj.krakow.pl:8080/publication/6109
| Edition name | Date |
|---|---|
| ZB-143571 | Feb 27, 2026 |
Karaś, Agnieszka
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Suski, Maciej
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