Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics

Congenital heart disease (CHD) is the most common birth defect in humans. It is a leading infant mortality factor worldwide, caused by defective cardiac development. Mutations in transcription factors, signalling and structural molecules have been shown to contribute to the genetic component of CHD....

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Main Authors: Granados-Riveron, Javier T., Brook, David
Format: Article
Published: Hindawi Publishing Corporation 2012
Online Access:https://eprints.nottingham.ac.uk/2589/
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author Granados-Riveron, Javier T.
Brook, David
author_facet Granados-Riveron, Javier T.
Brook, David
author_sort Granados-Riveron, Javier T.
building Nottingham Research Data Repository
collection Online Access
description Congenital heart disease (CHD) is the most common birth defect in humans. It is a leading infant mortality factor worldwide, caused by defective cardiac development. Mutations in transcription factors, signalling and structural molecules have been shown to contribute to the genetic component of CHD. Recently, mutations in genes encoding myofibrillar proteins expressed in the embryonic heart have also emerged as an important genetic causative factor of the disease, which implies that the contraction of the early heart primordium contributes to its morphogenesis. This notion is supported by increasing evidence suggesting that not only contraction but also formation, mechanosensing, and mechanotransduction of the cardiac myofibrillar proteins influence heart development. In this paper, we summarize the genetic clues supporting this idea.
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spelling nottingham-25892020-05-04T16:32:56Z https://eprints.nottingham.ac.uk/2589/ Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics Granados-Riveron, Javier T. Brook, David Congenital heart disease (CHD) is the most common birth defect in humans. It is a leading infant mortality factor worldwide, caused by defective cardiac development. Mutations in transcription factors, signalling and structural molecules have been shown to contribute to the genetic component of CHD. Recently, mutations in genes encoding myofibrillar proteins expressed in the embryonic heart have also emerged as an important genetic causative factor of the disease, which implies that the contraction of the early heart primordium contributes to its morphogenesis. This notion is supported by increasing evidence suggesting that not only contraction but also formation, mechanosensing, and mechanotransduction of the cardiac myofibrillar proteins influence heart development. In this paper, we summarize the genetic clues supporting this idea. Hindawi Publishing Corporation 2012-04-15 Article PeerReviewed Granados-Riveron, Javier T. and Brook, David (2012) Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics. Biochemistry Research International, 2012 (504906). pp. 1-6. ISSN 2090-2247 http://www.hindawi.com/journals/bri/2012/504906/ doi:10.1155/2012/504906 doi:10.1155/2012/504906
spellingShingle Granados-Riveron, Javier T.
Brook, David
Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title_full Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title_fullStr Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title_full_unstemmed Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title_short Formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
title_sort formation, contraction, and mechanotransduction of myofribrils in cardiac development: clues from genetics
url https://eprints.nottingham.ac.uk/2589/
https://eprints.nottingham.ac.uk/2589/
https://eprints.nottingham.ac.uk/2589/