| First Author | Means CW | Year | 2026 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 331 |
| Issue | 1 | Pages | H115-H129 |
| PubMed ID | 42222959 | Mgi Jnum | J:390116 |
| Mgi Id | MGI:8375882 | Doi | 10.1152/ajpheart.00007.2026 |
| Citation | Means CW, et al. (2026) Growth arrest of thoracic aortic aneurysms in aging Marfan mice. Am J Physiol Heart Circ Physiol 331(1):H115-H129 |
| abstractText | There remains a pressing need to identify pathological mechanisms that render a thoracic aortic aneurysm susceptible to continued enlargement, dissection, or rupture, yet additional insight can be gleaned by understanding compensatory mechanisms that limit disease progression and thereby stabilize a lesion. Our biomechanical data suggest that the ascending aorta within a common mouse model of Marfan syndrome, Fbn1(C1041G/+), exhibits progressive disease from 12 wk to 1 yr of age but near growth arrest from 1 to 2 yr of age. Comparison of the biomechanical phenotype, histological characteristics, and proteomic signature from 12 wk to 1 yr to 2 yr plus the transcriptional profile from 12 wk to 2 yr suggests that multiple differentially expressed genes (including downregulated Ltbp3 and Rictor) and associated proteins may contribute to late-term growth arrest. Although there is a need to better understand the interconnected roles of temporal changes in differential gene expression and protein abundance, modulating transforming growth factor-beta (TGF-beta) signaling and reducing mTOR signaling appear to merit increased attention in limiting aneurysmal expansion in Marfan syndrome.NEW & NOTEWORTHY Aneurysms in a mouse model of Marfan syndrome develop over the first year of life, only to stabilize over the second year of life. Remarkably, this paper is the first to identify, in a genetic condition of thoracic aortopathy, particular strategies that cells have identified to limit lesion growth and thus enhance resiliency. |
