Key result
Cardiomyocyte-specific Lonp1 deletion cuts cerebral blood flow ~43% in mice.
Why the study?
Does cardiac mitochondrial dysfunction induced by Lonp1 deletion impair brain mitochondrial function and cerebral blood flow in mice?
Population
Mice with induced heart failure via deletion of Lonp1 in cardiomyocytes, partial deletion of Lonp1, and…
Comparison
Deletion of Lonp1 in cardiomyocytes and partial… vs cre-control mice
Design
Preclinical
Follow-up
21 days
Authors
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Cardiac mitochondrial dysfunction in a mouse model of heart failure leads to reduced cerebral blood flow, brain mitochondrial metabolic remodeling, and cellular stress responses.
Does cardiac mitochondrial dysfunction induced by Lonp1 deletion impair brain mitochondrial function and cerebral blood flow in mice?
Absolute Event Rate: 587.1% vs 1034%
p-value: p=<0.0001
Cardiac mitochondrial dysfunction in a mouse model of heart failure leads to reduced cerebral blood flow, brain mitochondrial metabolic remodeling, and cellular stress responses.
Muthu et al. (2025) studied Heart failure. Cardiomyocyte-specific deletion of Lonp1 (Lonp1cKO) vs. cre-control and partial deletion of Lonp1 (Lonp1HetcKO) was evaluated on Cerebral blood flow (CBF) (p=<0.0001). Cardiomyocyte-specific deletion of Lonp1 in mice significantly reduced cerebral blood flow (587.1 vs 1034; p<0.0001) and impaired brain mitochondrial complex activities at 21 days.
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