Abstract
Background and Aims: Phenotypic modulation of smooth muscle cells (SMCs) promotes atherosclerosis, and the transition from quiescence to a proliferative state is a key feature of SMC plasticity. How SMCs regulate energy and biomass utilization during this transition is largely unknown. We previously showed that FAT1 intracellular domain (ICD) fragments localize to mitochondria, and that FAT1 expression in SMCs attenuates neointima formation after injury, in part by restraining cellular respiration.
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