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Type: Journal article
Title: Molecular mechanisms of atrial fibrosis: implications for the clinic
Author: Thanigaimani, S.
Lau, D.
Agbaedeng, T.
Elliott, A.
Mahajan, R.
Sanders, P.
Citation: Expert Review of Cardiovascular Therapy, 2017; 15(4):247-256
Publisher: Taylor & Francis
Issue Date: 2017
ISSN: 1477-9072
Statement of
Shivshankar Thanigaimani, Dennis H Lau, Thomas Agbaedeng, Adrian D. Elliott, Rajiv Mahajan and Prashanthan Sanders
Abstract: INTRODUCTION: Recent research has unravelled an increasing list of cardiac conditions and risk factors that may be responsible for the abnormal underlying atrial substrate that predisposes to atrial fibrillation (AF). Atrial fibrosis has been demonstrated as the pivotal structural abnormality underpinning conduction disturbances that promote AF in different disease models. Despite the advancement in our discoveries of the molecular mechanisms involved in the profibrotic milieu, targeted therapeutics against atrial fibrosis remain lacking. AREAS COVERED: This review is focused on detailing the key molecular signalling pathways that contribute to atrial fibrosis including: angiotensin II, transforming growth factor (TGF- ß1), connective tissue growth factor (CTGF) and endothelin-1. We also discussed the potential therapeutic options that may be useful in modulating the abnormal atrial substrate. In addition, we examined the new paradigm of AF care in lifestyle and risk factor management that has been shown to arrest and reverse the atrial remodelling process leading to improved AF outcomes. EXPERT COMMENTARY: The future of AF care is likely to require an integrated approach consisting of aggressive risk factor management in addition to the established paradigm of rate and rhythm management and anticoagulation. Translational studies on molecular therapeutics to combat atrial fibrosis is urgently needed.
Keywords: Atrial fibrillation
atrial fibrosis
atrial remodeling
molecular mechanisms
risk factor management
Rights: © 2017 Informa UK Limited, trading as Taylor & Francis Group
DOI: 10.1080/14779072.2017.1299005
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