Deficient ryanodine receptor S -nitrosylation increases sarcoplasmic reticulum calcium leak and arrhythmogenesis in cardiomyocytes

View Full Paper

Ask AI

Bookmark

Structured PICO

Population

NOS1(-/-), NOS1/NOS3(-/-), NOS3(-/-), and wild-type (WT) myocytes

Intervention

NOS1 deficiency (genetic knockout)

Comparator

Wild-type (WT) and NOS3(-/-) myocytes

Outcome

Diastolic Ca(2+) levels, Ca(2+) leak, spontaneous calcium waves, and RyR2 S-nitrosylationsurrogate

NOS1 deficiency causes RyR2 hyponitrosylation, leading to diastolic calcium leak and a proarrhythmic phenotype in cardiomyocytes.

No takes yet. Share an insight, caveat, or question.

Indicates NOS1 protects against diastolic Ca2+ leak in murine cardiomyocytes; leaves open relevance to human arrhythmias or therapies.

González et al. (2007) studied this question.

View Full Paper

Ask AI

Bookmark