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- W2590739844 abstract "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." @default.
- W2590739844 created "2017-03-03" @default.
- W2590739844 creator A5003136764 @default.
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- W2590739844 creator A5023691083 @default.
- W2590739844 creator A5024756348 @default.
- W2590739844 creator A5028738118 @default.
- W2590739844 creator A5041226897 @default.
- W2590739844 date "2017-03-08" @default.
- W2590739844 modified "2023-10-01" @default.
- W2590739844 title "Molecular mechanisms of atrial fibrosis: implications for the clinic" @default.
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