Nucleotide-binding domain and leucine-rich-repeat-containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung-like changes.

ABSTRACT: Mitochondrial dysfunction has long been implicated to have a causative role in organismal aging. A mitochondrial molecule, nucleotide-binding domain and leucine-rich-repeat-containing protein X1 (NLRX1), represents the only NLR family member that targets this cellular location, implying that NLRX1 probably establishes a fundamental link between mitochondrial functions and cellular physiology. However, the significance of NLRX1 function in cellular senescence, a key conceptual constituent in aging biology, is yet to be defined. Here, we demonstrate that molecular hallmarks involved in aging biology including NAD⁺ decline, and activation of mTOR, p53, and p16^INK4A are significantly enhanced in NLRX1 deficiency in vitro. Mechanistic studies of replicative cellular senesc

SUBMITTER: Shin HJ 

PROVIDER: S-EPMC8282248 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature