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Maladaptive repair post-AKI [driven by inflammation, hypoxia, interstitial fibrosis, and tubular injury (97)] promotes AKI-to-CKD transition, and ferroptosis is tightly linked to this process, highlighting its therapeutic potential

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MPT inhibition by NIM811 prevented cell death and/or mitochondrial depolarization after both high and low dose APAP, while the JNK inhibitor SP600125 decreased mitochondrial depolarization after low dose

Limitations of the molecular imaging studies conducted thus far include a lack of focus on treatment resistant depression, on depression subtypes including psychotic depression and menopausal depression, and the neurobiological mechanisms associated with other psychiatric and medical conditions comorbid with LLD, including substance use, pain and medical conditions including heart disease and diabetes