Polycystin-1 loss of function increases susceptibility to atrial fibrillation through impaired DNA damage response.
Troy HendricksonAbigail Abigail GieseMatthew FiedlerWilliam PerezErnesto Reyes-SanchezMonserrat Reyes-LozanoSufen WangLeslye Venegas-ZamoraVincent E ProvasekAschraf El-EssawiIngo BreitenbachFunsho E FakuadeIngo KutschkaGabriele G SchiattarellaNiels VoigtMiguel ValderrábanoFrancisco AltamiranoPublished in: bioRxiv : the preprint server for biology (2024)
Impaired PC1 increases in vivo AF inducibility under programmed electrical stimulation and promotes in vitro arrhythmias in hiPSC-aCM and HL-1 cells. Our findings indicate that PC1 protects against DNA damage to reduce AF susceptibility.
Keyphrases
- atrial fibrillation
- dna damage response
- dna damage
- dna repair
- induced apoptosis
- oral anticoagulants
- left atrial
- catheter ablation
- left atrial appendage
- oxidative stress
- direct oral anticoagulants
- cell cycle arrest
- heart failure
- spinal cord injury
- percutaneous coronary intervention
- endoplasmic reticulum stress
- congenital heart disease
- cell proliferation
- cell death
- coronary artery disease