Improved Understanding of the Pathology of Dwarfism May Lead to New Treatment Targets (IMAGE)

Elsevier

Improved Understanding of the Pathology of Dwarfism May Lead to New Treatment Targets

Caption

Misfolded protein accumulation stimulates endoplasmic reticulum (ER) stress, oxidative stress, and inflammation, creating a self-perpetuating cellular stress loop. Tumor necrosis factor (TNF)-α inflammation increases TNF-related apoptosis-inducing ligand (TRAIL) and midline 1 (MID1), which results in up-regulation of mammalian target of rapamycin complex 1 (mTORC1) signaling. mTORC1 signaling increases protein synthesis, which most likely exacerbates the stress on the already stressed ER. S6K1, protein S6 kinase beta-1; PERK, protein kinase-like endoplasmic reticulum kinase; CHOP, CCAAT/enhancer-binding protein homologous protein; AKT, protein kinase B; PP2A, protein phosphatase 2A.

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<i>American Journal of Pathology</i>

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