![TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology](https://www.ahajournals.org/cms/asset/d5382cfe-a3ff-456a-846c-70ed424ffbdc/hae0031103420005.jpg)
TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology
![Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv](https://www.biorxiv.org/content/biorxiv/early/2020/10/29/2020.10.28.360065/F7.large.jpg)
Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv
![Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv](https://www.biorxiv.org/content/biorxiv/early/2020/10/29/2020.10.28.360065/F5.large.jpg)
Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv
![TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology](https://www.ahajournals.org/cms/asset/a5c1b103-3f34-4420-b96e-d3da3febdfc3/hae0031103420003.jpg)
TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology
![TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology](https://www.ahajournals.org/cms/asset/ddfb913d-5330-44ba-98de-314f3397545a/hae0031103420006.jpg)
TGF-β1-Mediated Fibrosis and Ion Channel Remodeling Are Key Mechanisms in Producing the Sinus Node Dysfunction Associated With SCN5A Deficiency and Aging | Circulation: Arrhythmia and Electrophysiology
![Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv Enhanced diastolic dysfunction but preserved systolic function after acute pressure overload in the absence of smoothelin-like 1 protein | bioRxiv](https://www.biorxiv.org/content/biorxiv/early/2020/10/29/2020.10.28.360065/F1.large.jpg)