Cilia, mitochondria, and cardiac development
Bill Chaudhry and Deborah J. Henderson
Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Address correspondence to: Bill Chaudhry, Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, NE1 3BZ, United Kingdom. Phone: 44.191.241.8681; Email: bill.chaudhry@ncl.ac.uk.
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Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Address correspondence to: Bill Chaudhry, Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, NE1 3BZ, United Kingdom. Phone: 44.191.241.8681; Email: bill.chaudhry@ncl.ac.uk.
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First published June 17, 2019 - More info
J Clin Invest. 2019;129(7):2666–2668. https://doi.org/10.1172/JCI129827.
© 2019 American Society for Clinical Investigation
Motile cilia provide propulsion, and immotile ones are enriched with receptors. Both are required to establish left-right identity in the developing embryo and are also implicated in a wide range of human diseases. Abnormalities in cilial function underlie heterotaxy congenital heart disease (CHD) occurring in individuals with laterality disturbance. Mitochondrial function and cellular energetics, through mTOR and autophagy, are now linked with cilial function, revealing new mechanisms and candidate genes for syndromic human disease. In the current issue of the JCI, Burkhalter et al. ask the question: Can mitochondrial disturbances produce ciliopathy and does this explain some cases of heterotaxy?
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Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)