Key result
Cardiac stretch shows weak evidence for direct fibroblast activation, suggesting alternative mechanisms drive fibrosis.
Why the study?
Chronic atrial overload promotes AF via fibrosis, but evidence regarding whether cell stretch directly activates cardiac fibroblasts requires clarification.
This review reveals that the direct profibrotic effect of mechanical stretch on cardiac fibroblasts is weakly supported, pointing towards alternative mechanisms linking atrial overload to fibrosis in atrial fibrillation.
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Weakens support for direct stretch-fibroblast activation; leaves open alternative mechanisms linking cardiac overload to fibrosis.
Li et al. (2021) conducted a review in Atrial fibrillation and cardiac fibrosis. Cardiac stretch was evaluated. Evidence regarding direct fibroblast activation by stretch is weak and inconsistent, suggesting other mechanisms might account for the link between cardiac stretch and fibrosis.
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