October 9, 2025Circulation Research

Abstract Fri027: Fibroblast-specific NFκB-dependent signaling exacerbates inflammation and cardiac dysfunction in the heart following a myocardial infarction.

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NFκB deletion in fibroblasts improved cardiac function following myocardial infarction, indicating a protective role.
Ejection fraction and fractional shortening were restored in NFκB-deleted mice four weeks post-MI, highlighting the significance of fibrosis management.
Flow cytometry indicated lower inflammation levels due to NFκB deletion, showing its effect on immune cell recruitment.
Findings link fibroblast NFκB activation with the profibrotic TGF-β1/SMAD-3 pathway, emphasizing its critical role in cardiac remodeling.

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Implication

Experimental analysis reveals NFκB's role in exacerbating inflammation and cardiac dysfunction in mice after myocardial infarction, suggesting therapeutic potential.

Cite This Study

Singh et al. (2025) studied this question.

synapsesocial.com/papers/68e80eb363e2e2f707877d65 https://doi.org/10.1161/res.137.suppl_1.fri027

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Implication

Experimental analysis reveals NFκB's role in exacerbating inflammation and cardiac dysfunction in mice after myocardial infarction, suggesting therapeutic potential.

Abstract Fri027: Fibroblast-specific NFκB-dependent signaling exacerbates inflammation and cardiac dysfunction in the heart following a myocardial infarction.

Key Points

Discussion

Implication

Cite This Study

Abstract Fri027: Fibroblast-specific NFκB-dependent signaling exacerbates inflammation and cardiac dysfunction in the heart following a myocardial infarction.

Key Points

Discussion

Implication

Cite This Study

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