What does this research mean for the field?

Nicotine promotes atrial fibrillation and atrial fibrosis by downregulating miR-133 and miR-590, which leads to the upregulation of TGF-beta1 and TGF-betaRII. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the molecular mechanisms by which nicotine promotes atrial structural remodelling and increases vulnerability to atrial fibrillation.

April 27, 2009Cardiovascular ResearchOpen Access

Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

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Why the study?

Does nicotine administration promote atrial fibrillation and structural remodeling via miRNA regulation in a canine model?

Population

Canine model of atrial fibrillation and cultured canine atrial fibroblasts

Comparison

Nicotine administration vs Control (no nicotine)

Design

Preclinical

Follow-up

30 days

Authors

HSHongli ShanShanghai University YZYong ZhangInner Mongolia Agricultural University YLYanjie LuElectrophysiology

Discussion

Member takes

Implication

Nicotine may heighten AF risk via miRNA-fibrosis pathways; hypothesis-generating in canines, needs human validation.

Key Points

To determine the molecular mechanisms by which nicotine promotes atrial structural remodelling and increases vulnerability to atrial fibrillation.
Established an in vivo canine model of atrial fibrillation using 30-day nicotine administration combined with rapid pacing.
Treated cultured canine atrial fibroblasts with nicotine in vitro and manipulated miR-133 and miR-590 levels via transfection and antisense oligonucleotides.
Measured TGF-beta1, TGF-betaRII, and collagen expression while assessing the protective effect of an alpha7 nicotinic acetylcholine receptor antagonist.
Nicotine administration for 30 days increased atrial fibrillation vulnerability by approximately 8- to 15-fold and induced significant atrial fibrosis and collagen production in vivo and in vitro.
Nicotine decreased miR-133 and miR-590 levels by 60–70%, leading to the upregulation of their target proteins, TGF-beta1 and TGF-betaRII.
Transfection of miR-133 or miR-590 reduced TGF-beta1, TGF-betaRII, and collagen levels, whereas an alpha7 nicotinic acetylcholine receptor antagonist prevented nicotine's adverse effects.

Structured PICO

Does nicotine administration promote atrial fibrillation and structural remodeling via miRNA regulation in a canine model?

Population

Canine model of atrial fibrillation and cultured canine atrial fibroblasts

Intervention

Nicotine administration (in vivo for 30 days and in vitro)

Comparator

Control (no nicotine)

Outcome

Atrial fibrillation vulnerability, collagen production, and expression levels of TGF-beta1, TGF-betaRII, miR-133, and miR-590surrogate

Nicotine promotes atrial fibrosis and AF vulnerability in canines through the downregulation of miR-133 and miR-590, which normally repress profibrotic TGF-beta signaling.

Cite This Study

Shan et al. (2009) studied this question.

synapsesocial.com/papers/6a1bee67ea84844e355f2feb https://doi.org/10.1093/cvr/cvp130

Topics

Atrial fibrillation Persistent AF management

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Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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