Mutations in smooth muscle α-actin (ACTA2) lead to thoracic aortic aneurysms and dissections
Nature Genetics, ISSN: 1061-4036, Vol: 39, Issue: 12, Page: 1488-1493
2007
- 729Citations
- 307Captures
- 4Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations729
- Citation Indexes719
- 719
- CrossRef619
- Policy Citations7
- Policy Citation7
- Clinical Citations3
- PubMed Guidelines3
- Captures307
- Readers307
- 307
- Mentions4
- References4
- Wikipedia4
Article Description
The major function of vascular smooth muscle cells (SMCs) is contraction to regulate blood pressure and flow. SMC contractile force requires cyclic interactions between SMC α-actin (encoded by ACTA2) and the β-myosin heavy chain (encoded by MYH11). Here we show that missense mutations in ACTA2 are responsible for 14% of inherited ascending thoracic aortic aneurysms and dissections (TAAD). Structural analyses and immunofluorescence of actin filaments in SMCs derived from individuals heterozygous for ACTA2 mutations illustrate that these mutations interfere with actin filament assembly and are predicted to decrease SMC contraction. Aortic tissues from affected individuals showed aortic medial degeneration, focal areas of medial SMC hyperplasia and disarray, and stenotic arteries in the vasa vasorum due to medial SMC proliferation. These data, along with the previously reported MYH11 mutations causing familial TAAD, indicate the importance of SMC contraction in maintaining the structural integrity of the ascending aorta. © 2007 Nature Publishing Group.
Bibliographic Details
Springer Science and Business Media LLC
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