Ascending thoracic aortic aneurysms and dissections are fatal pathologies of the aorta. The study of physiopathological mechanisms highlights a medial degeneration characterized by extracellular matrix degradation and smooth muscle cells (SMC) dysregulation. However, pharmacological treatment does not reduce symptoms. Therefore, surgery currently remains the only means to treat aortic aneurysms and dissections. In this context, we focused on the potential roles of mitochondria as predictive factors. Mitochondria adapt their morphology to the physiological and energetic needs of the cell. This process is called mitochondrial dynamics and results from controlled cycles of mitochondrial fission (DRP1, FIS1) and fusion (OPA1, MFN1/2).

Our aim is to study mitochondrial homeostasis in aortic aneurysm and dissection as predictive factors for differentiation or worsening of the pathology.

Aortic tissue samples were obtained from a cohort of three patient groups (20/groups): control, aneurysm and dissection. Primary smooth muscle cells were extracted to determine mitochondrial network morphology by confocal microscopy using MitoTracker staining.

A decrease in mitochondrial size and shape, as well as in connectivity and mitochondrial network morphology, was observed in patients in the aneurysm group compared with the control and dissection groups. However, no differences in the expression of mitochondrial dynamics proteins were observed. An increase in mitophagy was observed in the aneurysm group, as well as a decrease in ATP synthase and a trend towards a decrease in respiratory chain complexes I and IV in the dissection group. In addition, preliminary results show mitochondrial DNA duplication in the dissection group.

These results tend to show differences between the aneurysm and dissection patient groups. These important and innovative results open new avenues of research into potential aggravation factors.