Key result
Aging drives ascending thoracic aortic stiffening, T-cell enrichment, and smooth muscle cell loss.
Maps mechanosensing changes in the ascending thoracic aorta, indicating aging impacts vascular health.
Aortic stiffening is an inevitable manifestation of chronological aging, yet the mechano-molecular programs that orchestrate region- and layer-specific adaptations along the length and through the wall of the aorta are incompletely defined. Here, we show that the decline in passive cyclic distensibility is more pronounced in the ascending thoracic (ATA) compared to distal segments of the aorta and that tissues in both the medial and adventitial compartments of the ATA stiffen during aging. Single-cell RNA sequencing of aged ATA tissues reveals altered cellular senescence, remodeling, and inflammatory responses accompanied by enrichment of T-lymphocytes and rarefaction of vascular smooth muscle cells, compared to young samples. T-lymphocytes accumulate in the adventitia and likely promote fibrosis, while activation of mechanosensitive piezo-1 enhances medial vasoconstriction. These results portray the immuno-mechanical aging of the ATA as a process that culminates in a stiffer conduit permissive to the accrual of multi-gerogenic signals priming to disease development.
No takes yet. Share an insight, caveat, or question.
Farra et al. (2022) studied Aortic stiffening. Aging vs. Young samples was evaluated on Transcriptomic and biomechanical changes in the ascending thoracic aorta. Aging leads to pronounced stiffening, altered cellular senescence, T-lymphocyte enrichment, and vascular smooth muscle cell rarefaction in the ascending thoracic aorta compared to young samples.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: