First-pass extracted concept

optogenetic defibrillation

Candidate: concept label1 source documents5 linked claims

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Evidence Snippets

we have tested optogenetic defibrillation using expression of the light-sensitive channel channelrhodopsin-2 (ChR2) in cardiac tissue

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2016Journal of Clinical InvestigationDOI PubMed

1 evidence snippet 5 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1application effectsupports2016Source 1DOI PubMed

Optogenetic defibrillation using cardiac ChR2 expression effectively terminated ventricular arrhythmias in mouse hearts.

Claim 2delivery enabled applicationsupports2016Source 1DOI PubMed

AAV-based gene transfer of ChR2 enabled effective optogenetic termination of ventricular arrhythmias in WT mouse hearts.

Claim 3mechanism of actionsupports2016Source 1DOI PubMed

Ventricular tachycardia termination was attributed to ChR2-mediated transmural depolarization that blocks voltage-dependent Na+ channels throughout the myocardial wall and interrupts wavefront propagation into illuminated tissue.

Claim 4simulation resultsupports2016Source 1DOI PubMed

In diseased ChR2-expressing human heart simulations, red light effectively terminated ventricular tachycardia.

Claim 5translational potentialsupports2016Source 1DOI PubMed

Optogenetic defibrillation could potentially be translated into humans to achieve nondamaging and pain-free termination of ventricular arrhythmia.