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Defective NOTCH signaling drives increased vascular smooth muscle cell apoptosis and contractile differentiation in bicuspid aortic valve aortopathy: a review of the evidence and future directions

Defective NOTCH signaling drives increased vascular smooth muscle cell apoptosis and contractile differentiation in bicuspid aortic valve aortopathy: a review of the evidence and future directions
Defective NOTCH signaling drives increased vascular smooth muscle cell apoptosis and contractile differentiation in bicuspid aortic valve aortopathy: a review of the evidence and future directions
Bicuspid aortic valve (BAV) disease remains the most common congenital cardiac disease and is associated with an increased risk of potentially fatal aortopathy including aortic aneurysm and dissection. Mutations in the NOTCH1 gene are one of only a few genetic anomalies identified in BAV disease; however evidence for defective NOTCH signaling, and its involvement in the characteristic histological changes of VSMC apoptosis and differentiation in ascending aortae of BAV patients is lacking. This review scrutinizes the evidence for the interactions of NOTCH signaling, cellular differentiation and apoptosis in the context of aortic VSMCs and provides focus for future research efforts in the diagnosis of BAV aortopathy and prevention of catastrophic complications through NOTCH signaling manipulation.
1050-1738
61-68
Harrison, O.J.
1feda5d5-8833-4587-9800-93135b68135a
Visan, A.C.
82ed996b-69da-44d5-8d28-f327b1a96c96
Moorjani, N.
ce44e232-2a6e-4616-8341-837ad0446acb
Modi, A.
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Salhiyyah, K.
63ac0bb3-5b7d-4d9f-87e5-3a20ba738a6a
Torrens, C.
15a35713-0651-4249-8227-5901e2cfcd22
Ohri, S.K.
02e88beb-3b66-4a91-9a5f-109b7b014280
Cagampang, F.R.
7cf57d52-4a65-4554-8306-ed65226bc50e
Harrison, O.J.
1feda5d5-8833-4587-9800-93135b68135a
Visan, A.C.
82ed996b-69da-44d5-8d28-f327b1a96c96
Moorjani, N.
ce44e232-2a6e-4616-8341-837ad0446acb
Modi, A.
3f1018c0-f808-4b9d-ba38-e9c64eb83929
Salhiyyah, K.
63ac0bb3-5b7d-4d9f-87e5-3a20ba738a6a
Torrens, C.
15a35713-0651-4249-8227-5901e2cfcd22
Ohri, S.K.
02e88beb-3b66-4a91-9a5f-109b7b014280
Cagampang, F.R.
7cf57d52-4a65-4554-8306-ed65226bc50e

Harrison, O.J., Visan, A.C., Moorjani, N., Modi, A., Salhiyyah, K., Torrens, C., Ohri, S.K. and Cagampang, F.R. (2019) Defective NOTCH signaling drives increased vascular smooth muscle cell apoptosis and contractile differentiation in bicuspid aortic valve aortopathy: a review of the evidence and future directions. Trends in Cardiovascular Medicine, 29 (2), 61-68. (doi:10.1016/j.tcm.2018.06.008).

Record type: Article

Abstract

Bicuspid aortic valve (BAV) disease remains the most common congenital cardiac disease and is associated with an increased risk of potentially fatal aortopathy including aortic aneurysm and dissection. Mutations in the NOTCH1 gene are one of only a few genetic anomalies identified in BAV disease; however evidence for defective NOTCH signaling, and its involvement in the characteristic histological changes of VSMC apoptosis and differentiation in ascending aortae of BAV patients is lacking. This review scrutinizes the evidence for the interactions of NOTCH signaling, cellular differentiation and apoptosis in the context of aortic VSMCs and provides focus for future research efforts in the diagnosis of BAV aortopathy and prevention of catastrophic complications through NOTCH signaling manipulation.

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BAV review TCM - Accepted Manuscript
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2019 (65) Trends in Cardiovascular Medicine (NOTCH signalling in BAV)
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Accepted/In Press date: 8 June 2018
e-pub ahead of print date: 21 June 2018
Published date: 1 February 2019

Identifiers

Local EPrints ID: 424827
URI: http://eprints.soton.ac.uk/id/eprint/424827
ISSN: 1050-1738
PURE UUID: e3add679-1406-4114-ba6e-8625682d9341
ORCID for F.R. Cagampang: ORCID iD orcid.org/0000-0003-4404-9853

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Date deposited: 05 Oct 2018 11:48
Last modified: 16 Mar 2024 06:52

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Contributors

Author: O.J. Harrison
Author: A.C. Visan
Author: N. Moorjani
Author: A. Modi
Author: K. Salhiyyah
Author: C. Torrens
Author: S.K. Ohri
Author: F.R. Cagampang ORCID iD

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