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An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.

Genes of the MICOS complex are a major candidate pathway to be potentially linked to defects in cardiomyocyte growth and differentiation in Hypoplastic left heart syndrome (HLHS), and relevant for elucidating the polygenic nature of HLHS and other CHDs.

A trial of mitofusin activation shows neuron regeneration and phenotype reversal in vitro and in vivo in experimental Charcot–Marie–Tooth disease type 2A caused by mitofusin 2 mutations.

Loss of FAD stemming from cell autonomous defects in mitochondrial proline catabolism impairs sperm quality male reproductive advantage in C. elegans.

A potential medication has been found for the brain and muscle degenerative diseases caused by mutant forms of Valosin-Containing Protein.

AAV-Txnip prolongs vision in mouse models of blindness, enhancing lactate catabolism, mitochondrial health, and ATP production in a condition that likely has a limited glucose supply.

Skeletal muscle from world-class octogenarian athletes, representing a population with very high physical function in advanced age, exhibits greater mass and strength that is associated with overrepresentation of proteins involved in mitochondrial biology and more oxidatively competent muscle fibers.

The double helix actin network surrounding the mitochondrial sheath of the sperm midpiece undergoes structural changes prior to the motility cessation during sperm-egg fusion.

Mitochondria reach stable positions in dendrites during a critical developmental period of high motility.