January 1, 2013Circulation JournalOpen Access

Role of Tumor Necrosis Factor-α in the Pathogenesis of Atrial Fibrosis and Development of an Arrhythmogenic Substrate

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Population

mice

Design

Preclinical

Authors

RLReginald LiewMount Elizabeth Hospital KKKatwadi KhairunnisaNewcastle University Medicine Malaysia YGYacui GuNational Heart Centre Singapore

Discussion

Member takes

Implication

May implicate TNF-α inhibition as AF therapeutic target; hypothesis-generating in mice and leaves clinical translation open.

Structured PICO

Population

mice

Intervention

Tumor Necrosis Factor-α (TNF-α) pathway evaluation

Outcome

Pathogenesis of atrial fibrosis, altered connexin-40 expression, and development of an arrhythmogenic substratesurrogate

TNF-α contributes to the development of an arrhythmogenic substrate and atrial fibrillation in mice through TGF-β signaling, myofibroblast activation, and MMP secretion.

Cite This Study

Liew et al. (2013) studied this question.

synapsesocial.com/papers/69d573169d980f6498ccb2a4 https://doi.org/10.1253/circj.cj-12-1155

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Role of Tumor Necrosis Factor-α in the Pathogenesis of Atrial Fibrosis and Development of an Arrhythmogenic Substrate

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Role of Tumor Necrosis Factor-α in the Pathogenesis of Atrial Fibrosis and Development of an Arrhythmogenic Substrate

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider