Ontology highlight
ABSTRACT: Rationale
FHFs (fibroblast growth factor homologous factors) are key regulators of sodium channel (NaV) inactivation. Mutations in these critical proteins have been implicated in human diseases including Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy. The underlying ionic mechanisms by which reduced Nav availability in Fhf2 knockout (Fhf2KO) mice predisposes to abnormal excitability at the tissue level are not well defined.Objective
Using animal models and theoretical multicellular linear strands, we examined how FHF2 orchestrates the interdependency of sodium, calcium, and gap junctional conductances to safeguard cardiac conduction.Methods and results
Fhf2KO
SUBMITTER: Park DS
PROVIDER: S-EPMC7718431 | biostudies-literature | 2020 Dec
REPOSITORIES: biostudies-literature