Key result
Genetic ablation of Ano5 in mice did not cause overt skeletal or cardiac muscle pathology and did not significantly alter maximal tetanic contraction force compared to wild-type mice.
Why the study?
Does genetic disruption of Ano5 cause skeletal or cardiac muscle pathology in mice?
Population
Ano5-knockout (KO) mice and wild type (WT) C57BL/6J mice
Comparison
Genetic disruption of Ano5; subset treated with… vs Wild type (WT) mice
Design
Preclinical
Follow-up
up to 18 months of age
Authors
Loading...
Mouse Ano5 KO fails to model human LGMD2L pathology; leaves open species differences and need for refined models.
Does genetic disruption of Ano5 cause skeletal or cardiac muscle pathology in mice?
Absolute Event Rate: 345.7% vs 374.8%
p-value: p=0.62
Genetic ablation of Ano5 in mice does not cause overt skeletal or cardiac muscle pathology, failing to recapitulate human ANO5-deficient muscular dystrophy, though it alters lipid metabolism and inflammation signaling.
Xu et al. (2015) studied ANO5-deficient muscular dystrophy. Genetic disruption of Ano5 (Ano5-knockout) vs. Wild type (WT) mice was evaluated on Maximal force during tetanic contraction at 150 Hz (mN/mm2) (p=0.62). Genetic ablation of Ano5 in mice did not cause overt skeletal or cardiac muscle pathology and did not significantly alter maximal tetanic contraction force compared to wild-type mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: