Katsuhiko Funai

This study shows that lactate can be directly imported into mitochondria and oxidized to support cardiac energy production, independent of the pyruvate carrier.

This study shows that mitochondrial cardiolipin deficiency disrupts electron transport chain function, leading to oxidative stress and promoting MASH in mice and humans.

This study shows that semaglutide causes muscle loss in male ob/ob mice but not in female ob/ob mice, revealing sex-specific effects on skeletal muscle mass and metabolism.

This study shows a high-fat, high-salt diet induces early MDAKD-like kidney injury in mice, with strain-specific mitochondrial dysfunction and fibrosis.

This study shows that N-acetylcarnosine treatment improves survival and delays age-related decline in multiple organ systems in female mice.

This study shows PGC-1α overexpression in skeletal muscle changes mitochondrial lipid composition but does not improve ATP synthesis efficiency.

The paper develops a method to profile mitochondrial function in specific kidney segments from mice and humans under thermodynamic control, revealing segment-specific bioenergetic differences.

This study shows semaglutide improves mitochondrial energy efficiency in skeletal muscle by enhancing ATP production per oxygen consumed during weight loss.

This study investigates whether muscle-specific Keap1 deletion prevents inactivity-induced muscle atrophy in mice, finding it enhances force production but does not prevent atrophy or weakness after hindlimb unloading.

This study shows that the MuSK-BMP pathway regulates Nav1.4 localization and muscle excitability at the neuromuscular junction, with implications for congenital myasthenic syndromes and aging.

This study shows that six months of physical inactivity in C57BL/6J mice on a high-fat diet does not cause chronic kidney disease but leads to early kidney injury markers.

This study investigates whether lipid peroxidation mediates muscle atrophy caused by PSD deficiency and finds that it does not.

The paper identifies a network of imprinted and non-imprinted genes that propagate parent-of-origin effects on metabolic traits through epistatic interactions in mice.

The paper identifies epistatic gene interactions underlying parent-of-origin effects on metabolic traits in mice using reciprocal crosses and tissue-specific expression analysis.