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dc.contributor.authorKassab, Sarah
dc.contributor.authorAlbalawi, Zainab
dc.contributor.authorDaghistani, Hussam
dc.contributor.authorKitmitto, Ashraf; email: ashraf.kitmitto@manchester.ac.uk
dc.date.accessioned2021-07-20T13:49:28Z
dc.date.available2021-07-20T13:49:28Z
dc.date.issued2021-07-02
dc.date.submitted2021-03-31
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625288/fcvm-08-689101.xml?sequence=2
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625288/fcvm-08-689101.pdf?sequence=3
dc.identifierhttps://chesterrep.openrepository.com/bitstream/handle/10034/625288/additional-files.zip?sequence=4
dc.identifier.citationFrontiers in Cardiovascular Medicine, volume 8, page 689101
dc.identifier.urihttp://hdl.handle.net/10034/625288
dc.descriptionFrom Frontiers via Jisc Publications Router
dc.descriptionHistory: collection 2021, received 2021-03-31, accepted 2021-06-08, epub 2021-07-02
dc.descriptionPublication status: Published
dc.description.abstractA pathophysiological consequence of both type 1 and 2 diabetes is remodelling of the myocardium leading to the loss of left ventricular pump function and ultimately heart failure (HF). Abnormal cardiac bioenergetics associated with mitochondrial dysfunction occurs in the early stages of HF. Key factors influencing mitochondrial function are the shape, size and organisation of mitochondria within cardiomyocytes, with reports identifying small, fragmented mitochondria in the myocardium of diabetic patients. Cardiac mitochondria are now known to be dynamic organelles (with various functions beyond energy production); however, the mechanisms that underpin their dynamism are complex and links to motility are yet to be fully understood, particularly within the context of HF. This review will consider how the outer mitochondrial membrane protein Miro1 (Rhot1) mediates mitochondrial movement along microtubules via crosstalk with kinesin motors and explore the evidence for molecular level changes in the setting of diabetic cardiomyopathy. As HF and diabetes are recognised inflammatory conditions, with reports of enhanced activation of the NLRP3 inflammasome, we will also consider evidence linking microtubule organisation, inflammation and the association to mitochondrial motility. Diabetes is a global pandemic but with limited treatment options for diabetic cardiomyopathy, therefore we also discuss potential therapeutic approaches to target the mitochondrial-microtubule-inflammatory axis.
dc.languageen
dc.publisherFrontiers Media S.A.
dc.rightsLicence for this article: http://creativecommons.org/licenses/by/4.0/
dc.sourceeissn: 2297-055X
dc.subjectCardiovascular Medicine
dc.subjectdiabetic cardiomyopathy
dc.subjectheart failure
dc.subjectMiro1
dc.subjectmicrotubules
dc.subjectHDAC6
dc.subjectNLRP3
dc.subjectmitochondrial dysfunction
dc.subjectmitochondrial movement
dc.titleMitochondrial Arrest on the Microtubule Highway—A Feature of Heart Failure and Diabetic Cardiomyopathy?
dc.typearticle
dc.date.updated2021-07-20T13:49:27Z
dc.date.accepted2021-06-08


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