Akt mitigates ER stress-instigated cardiac dysfunction via regulation of ferroptosis and mitochondrial integrity in a DHODH-dependent manner. (PubMed, Life Sci) - Apr 1, 2025 - "ER stress-induced myocardial anomalies were reversed by the newly identified PI3K activator triptolide, DHODH activator menaquinone-4 and pyrimidine booster coenzyme Q. In vitro experiment revealed that Akt activation- or triptolide-evoked beneficial responses against tunicamycin-induced cardiomyocyte anomalies were cancelled off by DHODH inhibitor BAY2402234 or ferroptosis inducer erastin. These findings support that chronic Akt activation rescues ER stress-evoked myocardial derangements through DHODH-dependent control of ferroptosis and mitochondrial homeostasis."
Journal • Fibrosis • Immunology • DDIT3 • GPX4 • HSPA5 • SLC7A11
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Dandan Hu; Jie Lin; Jun Ren; Kaishou Xu; Li Ma; Na Zhou; Russel J Reiter; Wanting Shi; Yingmei Zhang
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